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Obstentrics_Williams. Goplerud ], Eastman N]: Compound presentation: survey of 65 cases. Obstet Gynecol 1:59, 1953 Grobman WA, Bailit], Lai Y, et al: Association of the duration of active pushing with obstetric outcomes. Obstet Gynecol 12 (4):667, 2016 Handa VL, Laros RK: Active-phase arrest in labor: predictors of cesarean delivery in a nulliparous population. Obstet Gynecol 81 :758, 1993 Hannah M, Ohlsson A, Farine 0, et al: International Term PROM Trial: a RCT of induction of labor for prelabor rupture of membranes at term. Am J Obstet Gynecol 174:303, 1996 Hannah ME, Hodnett ED, Willan A, et al: Prelabor rupture of the membranes at term: expectant management at home or in hospital? Obstet Gynecol 96:533, 2000 Hansen SL, Clark SL, Foster JC: Active pushing versus passive fetal descent in the second stage of labor: a randomized controlled trial. Obstet Gynecol 99:29,r2002


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Obstentrics_Williams. Hansen SL, Clark SL, Foster JC: Active pushing versus passive fetal descent in the second stage of labor: a randomized controlled trial. Obstet Gynecol 99:29,r2002 Harper LM, Caughey AB, Roehl A, et al: Deining an abnormal irst stage of labor based on maternal and neonatal outcomes. m J Obstet Gynecol 210(6):536.el,r2014 Hauth )C, Hankins GO, Gilstrap LC III: Uterine contraction pressures achieved in parturients with active phase arrest. Obstet Gynecol 78:344, 1991 Hauth )C, Hankins GO, Gilstrap LC III, et al: Uterine contraction pressures with oxytocin induction/augmentation. Obstet GynecoI68:305, 1986 Hellman LM, Epperson )W, Connally F: Face and brow presentation: the experience of the Johns Hopkins Hospital, 1896 to 1948. Am ) Obstet Gynecol 59:831, 1950 Hendricks CH, Quilligan E), Tyler AB, et al: Pressure relationships between intervillous space and amniotic fluid in human term pregnancy. Am ) Obstet Gynecol77:1028, 1959


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Obstentrics_Williams. Hendricks CH, Quilligan E), Tyler AB, et al: Pressure relationships between intervillous space and amniotic fluid in human term pregnancy. Am ) Obstet Gynecol77:1028, 1959 Hillis OS: Diagnosis of contracted pelvis by the impression method. Surg Gynecol Obstet 51:857,o1930 Johnson CE: Transverse presentation of the fetus. )MA 187:642,o1964 Kaltreider OF: Criteria of midplane contraction. Am) Obstet GynecoI63:392, 1952 Korhonen U, Taipale P, Heinonen S: Fetal pelvic index to predict cephalopelvic disproportion-a retrospective clinical cohort study. Acta Obstet Gynecol Scand 94(6):615, 2015 Kwok CS, Judkins CL, Sherratt M: Forearm injury associated with compound presentation and prolonged labour.o) Neonatal Surg 4(3):40,o2015 Larks SO: Electrohysterography. Springfield, Thomas, 1960 Laughon SK, Berghella V, Reddy UM, et a1: Neonatal and maternal outcomes with prolonged second stage oflabor. Obstet Gynecol 124(1):57,2014


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Obstentrics_Williams. Laughon SK, Berghella V, Reddy UM, et a1: Neonatal and maternal outcomes with prolonged second stage oflabor. Obstet Gynecol 124(1):57,2014 Le Ray C, Audibert F, Goinet F, et al: When to stop pushing: efects of duration of second-stage expulsion eforts on maternal and neonatal outcomes in nulliparous women with epidural analgesia. Amo) Obstet Gynecol 201(4):361.e1,o2009 Leveno K), Nelson DB, McIntire DO: Second-stage labor: how long is too long? Am) Obstet Gynecol 214(4):484, 2016 Mahon TR, Chazotte C, Cohen WR: Short labor: characteristics and outcome. Obstet Gynecol 84:47, 1994 Manyonda IT, Shaw DE, Drife )0: he efect of delayed pushing in the second stage of labor with continuous lumbar epidural analgesia. Acta Obstet Gynecol Scand 69:291, 1990 Marte K, Voutsos L: Reduction in the cesarean delivery rate after obstetric care consensus guideline implementation. Obstet Gynecol 128(6):1445,o2016 Martin )A, Hamilton BE, Osterman M), et al: Births: final data for 2013. Nat!


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Obstentrics_Williams. Vital Stat Rep 64(1):1, 2015 McCarthy S: Magnetic resonance imaging in obstetrics and gynecology. Magn Reson Imaging 4:59, 1986 Mengert F: Estimation of pelvic capaciry.o)1A 138:169, 1948 Menticoglou SM, Manning F, Harman C, et 1: Perinatal outcomes in relation to second-stage duration. Am ) Obstet Gynecol 173:906, 1995a Menticoglou SM, Perlman M, Manning FA: High cervical spinal cord injury in neonates delivered with forceps: report of 15 cases. Obstet Gynecol 86:589, 1995b Moore MM, Shearer DR: Fetal dose estimates for CT pelvimetry. Radiology 171:265,o1989 Mozurkewich E, Chilimigras ), Koepke E, et al: Indications for induction of labour: a best-evidence review. B)OG 116(5):626,o2009 Mueller P: About the prognosis for delivery with a narrow pelvis. Arch GynaekoIo27:311, 1885


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Obstentrics_Williams. Mueller P: About the prognosis for delivery with a narrow pelvis. Arch GynaekoIo27:311, 1885 Nelson DB, McIntire DO, Leveno K): Relationship of the length of the first stage oflabor to the length of the second stage. Obstet GynecoIo122:27, 2013 Olah KS, Neilson ): Failure to progress in the management of labour. B)OG 101:1, 1994 Passos F, Cardose K, Coelho M, et a1: Antibiotic prophylaxis in premature rupture of membranes at term. Obstet GynecoIo120:1045, 2012 Pattinson RC, Cuthbert A, Vannevel V: Pelvimetry for fetal cephalic presentations at or near term for deciding on mode of delivery. Cochrane Database Syst Rev 3:CD000161, 2017 Peleg 0, Hannah ME, Hodnett ED, et 1: Predictors of cesarean delivery after prelabor rupture of membranes at term. Obstet Gynecol 93: 1 03o1, 1999 Plunkett BA, Lin A, Wong CA, et a1: Management of the second stage oflabor in nulliparas with continuous epidural analgesia. Obstet Gynecol 102:109, 2003


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Obstentrics_Williams. Plunkett BA, Lin A, Wong CA, et a1: Management of the second stage oflabor in nulliparas with continuous epidural analgesia. Obstet Gynecol 102:109, 2003 Reynolds SR, Heard 00, Bruns P, et 1: A multichannel strain-gauge tocodynamometer: an instrument for studying patterns of uterine contractions in pregnant women. Bull Johns Hopkins Hosp 82:446, 1948 Rosenbloom )1, Stout M), Tuuli MG, et al: New labor management guidelines and changes in cesarean delivery patterns. m)Obstet Gynecol October 14, 2017 [Epub ahead of print] Roshanfekr 0, Blakemore K), Leeo), et 1: Station at onset of active labor in nulliparous patients and risk of cesarean delivery. Obstet Gynecol 93:329, 1999 Rouse D), Oweno), Hauth ]C: Active-phase labor arrest: oxytocin augmenta tion for at least 4 hours. Obstet Gynecol 93:323, 1999 Rouse D), Weiner S), Bloom SL, et a1: Second-stage labor duration in nulliparous women: relationship to maternal and perinatal outcomes. Am ) Obstet GynecoIo201(4):357.e1,o2009


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Obstentrics_Williams. Rouse D), Weiner S), Bloom SL, et a1: Second-stage labor duration in nulliparous women: relationship to maternal and perinatal outcomes. Am ) Obstet GynecoIo201(4):357.e1,o2009 Satin A), Maberry lC, Leveno ), et al: Chorioamnionitis: a harbinger of dystocia. Obstet Gynecol 79:913, 1992 Shafer BL, Cheng W, Vargas ]E, et a1: Face presentation: predictors and delivery route. Am] Obstet Gynecol 194(5):elO, 2006 Sharma SK, McIntire DO, Wiley), et al: Labor analgesia and cesarean delivery: an individual patient meta-analysis of nulliparous women. Anesthesiology 100(1):142,o2004 Sheiner E, Levy A, Mazor M: Precipitate labor: higher rates of maternal complications. Euro] Obstet Gynecol Reprod BioI 116(1):43, 2004 Sporri S, Hanggi W, Brahetti A, et a1: Pelvimetry by magnetic resonance imaging as a diagnostic tool to evaluate dystocia. Obstet Gynecol 89:902, 1997 Stark DO, McCarthy SM, Filly A, et a1: Pelvimetry by magnetic resonance imaging. Am) RadioIo144:947, 1985


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Obstentrics_Williams. Tebes CC, Mehta P, Calhoun DA, et 1: Congenital ischemic forearm necrosis associated with a compound presentation. ] Matern Fetal Med 8:281, 1999 Thoms H: he obstetrical signiicance of pelvic variations: a study of 450 primiparous women. Bl] 2:210, 1937 Thorpo)M )r, Pahel-Short L, Bowes WAo)r: The Mueller-Hillis maneuver: can it be used to predict dystocia? Obstet Gynecol 82:5o19, 1993 Thurnau GR, Scates DH, Morgan MA: he fetal-pelvic index: a method of identiying fetal-pelvic disproportion in women attempting vaginal birth after previous cesarean delivery. Am) Obstet Gynecol 165:353, 1991 Vallier A, Cureton BA, Schubeck 0: Pregnancy outcomes ater pelvic ring injury.o) Orthop Trauma 26(5):302,o2012 Wilson-Leedy ]G, DiSilvestro A), Repke ]T, et al: Reduction in the cesarean delivery rate after Obstetric Care Consensus guideline implementation. Obstet GynecoIo128(1):145, 2016


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Obstentrics_Williams. Wilson-Leedy ]G, DiSilvestro A), Repke ]T, et al: Reduction in the cesarean delivery rate after Obstetric Care Consensus guideline implementation. Obstet GynecoIo128(1):145, 2016 Wong CA, Scavone BM, Dugan S, et 1: Incidence of postpartum lumbosacral spine and lower extremiry nerve injuries. Obstet Gynecol 101o:279,o2003 World Health Organization: Partographic management of labour. Lancet 343:1399, 1994 Zaretsky MV, Alexander ]M, McIntire DO, et al: Magnetic resonance imaging pelvimetry and the prediction of labor dystocia. Obstet Gynecol 106:919, 2005 Zhango), Landy H), Branch OW, et al: Contemporary patterns of spontaneous labor with normal neonatal outcomes. Obstet Gynecol 116: 1281, 2010 Zhang], Troendle ]F, Yancey MK: Reassessing the labor curve in nulliparous women. m) Obstet GynecoIo187(4):824, 2002 ELECTRONIC FETAL MONITORING ................. 457 OTHER INTRAPARTUM ASSESSMENT TECHNIQUES ... 470 NONREASSURING FETAL STATUS ................. 472


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Obstentrics_Williams. ELECTRONIC FETAL MONITORING ................. 457 OTHER INTRAPARTUM ASSESSMENT TECHNIQUES ... 470 NONREASSURING FETAL STATUS ................. 472 MECONIUM IN THE AMNIONIC FLUID .............. 474 FETAL HEART RATE PAIERNS AND BRAIN INJURY ... 476 CURRENT RECOMMENDATIONS ................... 478 INTRAPARTUM SURVEILLANCE OF UTERINE ACTIVIY ... 478 To study the orces exerted by labour, a rubber bag was inserted into the uterus which was connected with a manometer. In this way it was ound that the intra-uterine pressure, in the intervals between the contractions, was represented by a column of mercury 20 millimeters high, 5 of which were due to the toniciy of the wals and 15 to its contents. During the pains, however, the mercury rose consideraby, reaching a height of from 80 to 250 milimeters. -J. Whitridge Williams (1903)


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Obstentrics_Williams. -J. Whitridge Williams (1903) Little is written in the first edition of this textbook concerning monitoring of the fetus during labor. Much later, periodic auscultation of the fetal heartbeat with a fetoscope was adopted. These practices were eclipsed in the late 1960s and early 1970s by the development of electronic fetal monitoring (Hon, 1958). It was hoped that the continuous graph-paper portrayal of the fetal heart rate was potentially diagnostic in assessing pathophysiological events afecting the fetus. When first introduced, electronic fetal heart rate monitoring was used primarily in complicated pregnancies but gradually became used in most pregnancies. Now, more than 85 percent of all live births in the United States undergo electronic fetal monitoring (Ananth, 2013). Direct fetal heart measurement is accomplished by attaching a bipolar spiral electrode directly to the fetus (Fig.


Obstentrics_Williams

Obstentrics_Williams. Direct fetal heart measurement is accomplished by attaching a bipolar spiral electrode directly to the fetus (Fig. The wire electrode penetrates the fetal scalp, and the second pole is a metal wing on the electrode. The electrical fetal cardiac signal-P wave, QRS complex, and T wave-is ampliied and must be applied because air conducts ultrasound waves poorly. he device Mother 50 mm/sec FIGURE 24-1 Internal electronic fetal monitoring. Schematic representation of a bipolar electrode attached to the fetal scalp for detection of fetal QRS complexes (F). Also shown is the maternal heart and corresponding electrical complex (M) that is detected. is held in position by an elastic belt.


Obstentrics_Williams

Obstentrics_Williams. is held in position by an elastic belt. FIGURE 24-3 The top tracing shows standard fetal monitor tracing of heart rate using a fetal scalp electrode, Spiking ofthe fetal rate in the monitor tracing is due to premature atrial con entiation of fetal cardiac motion from tractions, The second panel displays accompanying contractions, The bottom two tracings repmaternal arterial pulsations (Neilson, resent cardiac electrical complexes detected from fetal scalp and maternal chest wall electrodes, 2008). ECG = electrocardiogram; F = fetus; M = mother; PAC = fetal premature atrial contraction, fed into a cardiotachometer for heart rate calculation. he peak R-wave voltage is the portion of the fetal electrocardiogram (ECG) most reliably detected.


Obstentrics_Williams

Obstentrics_Williams. n example of the method of fetal heart rate processing employed when a scalp electrode is used is shown in Figure 24-2. Time (t) in milliseconds between fetal R waves is fed into a cardiotachometer, where a new fetal heart rate is set with the arrival ofeach new R wave. As also shown in Figure 24-2, a premature atrial contraction is computed as a heart rate acceleration because the interval (t2) is shorter than the preceding one (t1). he phenomenon of continuous R-to-R wave fetal heart rate computation is known as beat-to-beat variabiliy.


Obstentrics_Williams

Obstentrics_Williams. Electrical cardiac complexes detected by the electrode include those generated by the mother. However, the amplitude of the maternal ECG signal is diminished when recorded through the fetal scalp electrode and is masked by the fetal ECG. Shown in Figure 24-3 are simultaneous recordings of maternal chest wall ECG signals and fetal scalp electrode ECG signals. This fetus is experiencing premature atrial contractions, which cause the cardiotachometer to rapidly and erratically seek new heart rates, resulting in the "spiking" shown in the standard fetal monitor tracing. Importantly, when the fetus is dead, the maternal R waves are still detected by the scalp electrode as the next best signal and are counted by the cardiotachometer (Fig. 24-4).


Obstentrics_Williams

Obstentrics_Williams. Although membrane rupture may be avoided, external monitoring does not provide the precision of fetal heart rate measurement aforded by internal monitoring (Nunes, 2014). In some women-for example, those who are obese-external monitoring may be dificult (Brocato, 2017). With external monitoring, the fetal heart rate is detected through the maternal abdominal wall using the ultrasound Doppler principle. Ultrasound waves undergo a shift in frequency as they are reflected from moving fetal heart valves and from pulsatile blood ejected during systole (Chap. 10, p. 213). he unit consists of a transducer that emits ultrasound and a sensor to detect a shift in frequency of the reflected sound. The transducer is placed on the maternal abdomen at a site where fetal heart action is best detected. A coupling gel


Obstentrics_Williams

Obstentrics_Williams. FIGURE 24-2 Schematic representation offetal electrocardiographic signals used to compute continuing beat-to-beat heart rate with scalp electrodes, Time intervals (tIl t21 t3) in milliseconds between successive fetal R waves are used by a cardiotachometer to compute instantaneous fetal heart rate, ECG = electrocardiogram; PAC = premature atrial contraction, contractions. FIGURE 24-4 Placental abruption. In the upper panel, the fetal scalp electrode first detected the heart rate of the dying fetus. After fetal death, the maternal electrocardiogram complex is detected and recorded. The second panel displays an absence of uterine


Obstentrics_Williams

Obstentrics_Williams. Ultrasound Doppler signals are edited electronically before fetal heart rate data are printed onto monitor paper. Relected ultrasound signals from moving fetal heart valves are analyzed through a microprocessor that compares incoming signals with the most recent previous signal. This process, called autocorrelation, is based on the premise that the fetal heart rate has regularity, whereas "noise" is random and without regularity. Several fetal heart motions must be deemed electronically acceptable by the microprocessor before the fetal heart rate is printed. Such electronic editing has greatly improved the tracing quality of the externally recorded fetal heart rate. Other features of current fetal monitors include the capability to monitor twin fetuses, monitor concurrent maternal heart rate, display the fetal ECG, and record maternal pulse oximetry values. Many fetal monitors are capable of interfacing with archival storage systems, which obviates maintaining actual paper tracings.


Obstentrics_Williams

Obstentrics_Williams. Technological advances now allow fetal heart rate monitoring from a remote, centralized location. Theoretically, the ability to monitor several patients simultaneously was hoped to improve neonatal outcomes. That said, only one study on centralized fetal monitoring has been reported. Anderson and colleagues (2011) measured the ability of 12 individuals to detect critical signals in fetal heart rate tracings on one, two, or four monitors. The results showed that detection accuracy declined as the number of displays increased. The interpretation of fetal heart rate patterns can be problematic without deinitions and nomenclature. In one example, Blackwell and colleagues (2011) asked three .1aternal-Fetal Medicine specialists to independently interpret 154 fetal heart rate tracings. Interobserver agreement was poor for the most ominous tracings and moderate for less severe patterns.


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Obstentrics_Williams. The National Institute of Child Health and Human Development (NICHD) Research Planning Workshop (1997) brought together investigators with exper tise in the ield to propose standardized, tion of fetal heart rate patterns during labor. This workshop reconvened in 2008. he deinitions proposed as a result of this second workshop are used in this chapter and have been adopted by the American College of Obstetricians and Gynecolo Importantly, interpretation of electronic fetal heart rate data is based on the visual pattern of the heart rate as portrayed on chart recorder graph paper. Thus, the choice of vertical and horizontal scaling greatly afects the appearance of the fetal heart rate. Scal ing factors recommended by the NICHD


Obstentrics_Williams

Obstentrics_Williams. Workshop are 30 beats per minute (beats/ min or bpm) per vertical cm (range, 30 to paper speed. Fetal heart rate variation is falsely displayed at the slower 1 cm/ min paper speed compared with that of the smoother baseline recorded at 3 cm/min. hus, pattern recognition can be con siderably distorted depending on the scaling factors used. This refers to the modal characteristics that prevail apart from periodic accelerations or decelerations associated with uterine contractions. Descriptive characteristics of baseline fetal heart activity include rate, beat-to-beat variabili, etal arrhythmia, and distinct patterns such as sinusoidal or saltatory fetal heart rates.


Obstentrics_Williams

Obstentrics_Williams. With increasing fetal maturation, the heart rate decreases. This continues postnatally such that the average rate is 85 bpm by age 8 years (Tintinalli, 2016). Pillai and James (1990) reported that the baseline fetal heart rate declined an average of 24 bpm between 16 weeks' gestation and term, or approximately 1 bpm per week. his normal gradual slowing of the fetal heart rate is thought to correspond to maturation of parasympathetic (vagal) heart control (Renou, 1969).


Obstentrics_Williams

Obstentrics_Williams. The baseline fetal heart rate is the approximate mean rate rounded to increments of 5 bpm during a 10-minute tracing segment. In any 10-minute window, the minimum interpretable baseline duration must be at least 2 minutes. If the baseline fetal heart rate is less than 110 bpm, it is termed bradycardia . If the baseline rate is greater than 160 bpm, it is called tachycardia. The average fetal heart rate is considered the result of tonic balance between accelerator and decelerator influences on pacemaker cells. In this concept, the sympathetic system is the accelerator influence, and the parasympathetic system is the decelerator factor mediated by vagal slowing of heart rate (Dawes, 1985). Heart rate also is under the control of arterial chemoreceptors such that both hypoxia and hypercapnia can modulate rate. More severe and prolonged hypoxia, with a TABLE 24-' . Electronic Fetal Monitoring Definitions


Obstentrics_Williams

Obstentrics_Williams. TABLE 24-' . Electronic Fetal Monitoring Definitions Baseline • The mean FHR rounded to increments of 5 bpm during a 1 O-min segment, excluding: -Periods of marked FHR variability -Segments of baseline that difer by more than 25 bpm The baseline must be for a minimum of 2 min in any 1 O-min segment or the baseline for that time period is indeterminate. In this case, one may refer to the prior 1 O-min window for determination of baseline. Normal FHR baseline: 11s0-1s60 bpm Tachycardia: FHR baselines is greater than 160 beats per minute Bradycardia: FHR baseline is less than 11s0 beats per minute


Obstentrics_Williams

Obstentrics_Williams. Normal FHR baseline: 11s0-1s60 bpm Tachycardia: FHR baselines is greater than 160 beats per minute Bradycardia: FHR baseline is less than 11s0 beats per minute Baseline • Fluctuations in the baseline FHR that are irregular in amplitude and frequency variability • Variability is visually quantified as the amplitude of peak-to-trough in beats per minute -Absent: amplitude range undetectable -Minimal: amplitude range detectable but 5 beats per minutes or fewer -Moderate (normal): amplitude range 6-25 beats per minute -Marked: amplitude range greater than 25 beats per minute Acceleration • A visually apparent abrupt increase (onset to peak in less than 30 seconds) in the FHR At 32 weeks of gestation and beyond, an acceleration has a peak of 15 bpm or more above baseline, with a duration of 15 sec or more but less than 2 minutes from onset to return


Obstentrics_Williams

Obstentrics_Williams. At 32 weeks of gestation and beyond, an acceleration has a peak of 15 bpm or more above baseline, with a duration of 15 sec or more but less than 2 minutes from onset to return Before 32 weeks, an acceleration has a peak of 10 bpm or more above baseline, with a duration of 10 seconds or more but less than 2 minutes from onset to return If an acceleration lasts 10 minutes or longer, it is a baseline change Early deceleration • Visually apparent usually symmetrical gradual decrease and return of the FHR associated with a A gradual FHR decrease is defined as from the onset to the FHR nadir of 30 seconds or more The decrease in FHR is calculated from the onset to the nadir of the deceleration The nadir of the deceleration occurs at the same time as the peak of the contraction


Obstentrics_Williams

Obstentrics_Williams. The decrease in FHR is calculated from the onset to the nadir of the deceleration The nadir of the deceleration occurs at the same time as the peak of the contraction In most cases the onset, nadir, and recovery of the deceleration are coincident with the beginning, peak, and ending of the contraction, respectively Late deceleration • Visually apparent usually symmetrical gradual decrease and return of the FHR associated with a A gradual FHR decrease is defined as from the onset to the FHR nadir of 30 seconds or more The decrease in FHR is calculated from the onset to the nadir of the deceleration The deceleration is delayed in timing, with the nadir of the deceleration occurring after the peak of the contraction In most cases the onset, nadir, and recovery of the deceleration occur after the beginning, peak, and ending of the contraction, respectively deceleration • An abrupt FHR decrease is defined as from the onset of the deceleration to the beginning of the


Obstentrics_Williams

Obstentrics_Williams. FHR nadir of less than 30 seconds The decrease in FHR is calculated from the onset to the nadir of the deceleration The decrease in FHR is 15 beats per minute or greater, lasting 15 seconds or greater, and less than 2 minutes in duration When variable decelerations are associated with uterine contraction, their onset, depth, and duration commonly vary with successive uterine contractions Prolonged • Visually apparent decrease in the FHR below the baseline deceleration • Decrease in FHR from the baseline that is 15 per minute or more, and less than 2 minutes in duration • If a deceleration last 10 minutes or longer, it is a baseline change Sinusoidal pattern • Visually apparent, smooth, sine wave-line undulating pattern in FHR baseline with a cycle frequency of 3-5 per minute which persists for 20 dinutes or more FHR = fetal heart rate. Data from Macones, 2008.


Obstentrics_Williams

Obstentrics_Williams. FHR = fetal heart rate. Data from Macones, 2008. FIGURE 24-6 Schematic representation of short-term beat-tobeat variability measured by a fetal scalp electrode. t time interval between successive fetal R waves. (Adapted with permission from Klavan M, Laver AT, Boscola MA: Clinical concepts of fetal heart rate monitoring. Waltham, Hewlett-Packard, 1977.) FIGURE 24-5 Fetal bradycardia measured with a scalp electrode (upper paneD in a pregnancy complicated by placental abruption and subsequent fetal death. Concurrent uterine contractions are shown in the lower panel. rising blood lactate level and severe metabolic acidemia, induces a prolonged fall in heart rate (hakor, 2009).


Obstentrics_Williams

Obstentrics_Williams. rising blood lactate level and severe metabolic acidemia, induces a prolonged fall in heart rate (hakor, 2009). Bradycardia. In the third trimester, the normal mean baseline fetal heart rate has generally been accepted to range between 120 and 160 bpm. But, pragmatically, a rate between 100 and 119 bpm, in the absence of other changes, usually is not considered to represent fetal compromise. Such low but potentially normal baseline heart rates also have been attributed to head compression from occiput posterior or transverse positions, particularly during second-stage labor (Young, 1976). Such mild bradycardias were observed in 2 percent of monitored pregnancies and averaged approximately 50 minutes in duration. Freeman and associates (2003) have concluded that bradycardia within the range of 80 to 120 bpm and with good variability is reassuring. Interpretation of rates less than 80 bpm is problematic, and such rates generally are considered nonreassuring.


Obstentrics_Williams

Obstentrics_Williams. Some causes of fetal bradycardia include congenital heart block and serious fetal compromise 0aeggi, 2008; Larma, 2007). Figure 24-5 shows bradycardia in a fetus dying from placental abruption. Maternal hypothermia under general anesthesia for repair of a cerebral aneurysm or during maternal cardiopulmonary bypass for open-heart surgery can also cause fetal bradycardia. Sustained fetal bradycardia in the setting of severe pyelonephritis and maternal hypothermia also has been reported (Hankins, 1997). Involved fetuses apparently are not harmed by several hours of such bradycardia.


Obstentrics_Williams

Obstentrics_Williams. Tachycardia. Fetal tachycardia is deined as a baseline heart rate greater than 160 bpm. The most common explanation for fetal tachycardia is maternal fever from chorioamnionitis, although fever from any source can produce this. In some cases, fetal tachycardia may precede overt maternal fever (Gilstrap, 1987). Fetal tachycardia caused by maternal infection typically is not associated with fetal compromise unless there are associated periodic heart rate changes or fetal sepsis. Other causes of fetal tachycardia include fetal compromise, cardiac arrhythmias, and maternal administration of parasympathetic inhibiting (atropine) or sympathomimetic (terbutaline) drugs. Prompt relief of the compromising event, such as correction of maternal hypotension caused by epidural analgesia, can result in fetal recovery. he key feature to distinguish fetal compromise in association with tachycardia seems to be concomitant heart rate decelerations.


Obstentrics_Williams

Obstentrics_Williams. Wandering Baseline. This baseline rate is unsteady and "wanders" between 120 and 160 bpm (Freeman, 2003). This rare finding is suggestive of a neurologically abnormal fetus and may occur as a preterminal event. In contrast, changes of the normal baseline are common in labor and do not predict morbidity (Yang, 2017).


Obstentrics_Williams

Obstentrics_Williams. Baseline variability is an important index of cardiovascular function and appears to be regulated largely by the autonomic nervous system (Kozuma, 1997). That is, a sympathetic and parasympathetic "push and pull" mediated via the sinoatrial node produces moment-to-moment or beat-to-beat oscillation of the baseline heart rate. Such heart rate change is deined as baseline variability. Variability can be further analyzed over the short term and long term, although these terms have fallen out of use. Short-term variabiliy relects the instantaneous change in fetal heart rate from one beat-or R wave-to the next. This variability is a measure of the time interval between cardiac systoles (Fig. 24-6). Short-term variability can most reliably be determined to be normally present only when electrocardiac cycles are measured directly with a scalp electrode. Long-term variability is used to describe the oscillatory changes during 1 minute and result in the waviness of the baseline (Fig. 24-7).


Obstentrics_Williams

Obstentrics_Williams. FIGURE 24-7 Schematic representation of long-term beat-to-beat variability of the fetal heart rate ranging between 125 and 135 bpm. (Adapted with permission from Klavan M, Laver AT, Boscola MA: Clinical concepts of fetal heart rate monitoring. Waltham, HewlettPackard, 1977.) he normal frequency of such waves is three to ive cycles per minute (Freeman, 2003).


Obstentrics_Williams

Obstentrics_Williams. It should be recognized that precise quantitative analysis of both short-and long-term variability presents several frustrating problems due to technical and scaling factors (Parer, 1985). hus, most clinical interpretation is based on visual analysis with subjective judgment of the smoothness or latness of the baseline. According to Freeman and associates (2003), no evidence suggests that the distinction between short-and long-term variability has clinical relevance. Similarly, the NICHD Workshop (1997) did not recommend diferentiating short-and long-term variability because in actual practice they are visually determined as a unit. The workshop panel defined baseline variability as those baseline luctuations of two cycles per minute or greater. They recommended the criteria shown in Figure 24-8 for quantification of variability. Normal beatto-beat variability was accepted to be 6 to 25 bpm.


Obstentrics_Williams

Obstentrics_Williams. Increased Variability. Several physiological and pathological processes can afect beat-to-beat variability. Greater variability accompanies fetal breathing and body movements (Dawes, 1981; Van Geijn, 1980). Pillai and James (1990) reported increased baseline variability with advancing gestation. Up to 30 weeks, baseline characteristics were similar during both fetal rest and activity. After 30 weeks, fetal inactivity was associated with diminished baseline variability, but fetal activity enhanced it. Last, the baseline fetal heart rate becomes more physiologically ixed (less variable) as the rate rises. This phenomenon presumably relects less cardiovascular physiological wandering as beat-to-beat intervals shorten with a higher heart rate.


Obstentrics_Williams

Obstentrics_Williams. Decreased Variability. A common cause of diminished beatto-beat variability is administration of analgesic drugs during labor (Chap. 25, p. 487). Various central nervous system depressant drugs can cause transient diminished beat-to-beat variability. Included are narcotics, barbiturates, phenothiazines, tranquilizers, and general anesthetics. Corticosteroids also dampen variability (Knaven, 2017). As one specific example, variability regularly diminishes within 5 to 10 minutes following intravenous meperidine administration, and the efects may last up to 60 minutes or longer (Hill, 2003; Petrie, 1993). Butorphanol given intravenously has similar efects (Schucker, 1996). And, chronically administered buprenorphine suppresses fetal heart rate and movement (Jansson, 2017).


Obstentrics_Williams

Obstentrics_Williams. Magnesium suate, widely used in the United States for tocolysis or management of hypertensive gravidas, is associated with diminished beat-to-beat variability. In a study of nearly 250 term gestations, magnesium sulfate administration led to decreased variability but without evidence of adverse neonatal efects (Duy, 2012). Others have echoed these findings (Hallak, 1999; Lin, 1988). With magnesium sulfate tocolysis of preterm labor, variability was also diminished in most reviewed studies (Nensi, 2014; Verdurmen, 2017). Of greatest concern, diminished beat-to-beat variability can be an ominous sign indicating a seriously compromised fetus. Paul and coworkers (1975) reported that loss of variability in combination with decelerations was associated with etal acidemia. Decreased variability was deined as an excursion of the baseline of;5 bpm (see Fig. 24-8). Severe maternal acidemia can also lower fetal beat-to-beat variability, for example, in a mother with diabetic ketoacidosis.


Obstentrics_Williams

Obstentrics_Williams. According to Dawes (1985), metabolic acidemia that causes depression of the fetal brainstem or the heart itself creates the loss of variability. hus, diminished beat-to-beat variability, when it relects fetal compromise, likely relects acidemia rather than hypoxia. Indeed, mild degrees of fetal hypoxemia have been reported actually to enhance variability, at least initially (Murotsuki, 1997).


Obstentrics_Williams

Obstentrics_Williams. Reduced baseline heart rate variabiliy is the single most reliable sign of etal compromise. Smith and coworkers (1988) performed a computerized analysis of beat-to-beat variability in growth-restricted fetuses before labor. Diminished variability (;4.2 bpm) maintained for 1 hour was diagnostic of developing acidemia and imminent fetal death. In contrast, Samuelof and associates (1994) evaluated variability in 2200 consecutive deliveries and concluded that variability by itself could not be used as the only indicator of fetal well-being. They also warned that good variability should not be interpreted as necessarily reassuring. Blackwell and associates (2011) found that even experts often disagreed as to whether variability was absent or minimal (;5 bpm).


Obstentrics_Williams

Obstentrics_Williams. In sum, beat-to-beat variability is afected by fetal physiology, and its meaning difers depending on the clinical setting. Decreased variability in the absence of decelerations is unlikely to reflect fetal hypoxia (Davidson, 1992). A persistently flat fetal heart rate baseline-absent variability-within the normal baseline rate range and without decelerations may relect a previous fetal insult that has resulted in neurological damage (Freeman, 2003). When fetal cardiac arrhythmias are irst suspected using electronic monitoring, indings can include baseline bradycardia, tachycardia, or most commonly in our experience, abrupt baseline spiking (Fig. 24-9). An arrhythmia can only be documented, practically speaking, when scalp electrodes are used. Some fetal monitors can be adapted to output the scalp electrode signals into an ECG recorder. Because only a single lead is obtained, analysis and interpretation of rhythm and rate disturbances are severely limited.


Obstentrics_Williams

Obstentrics_Williams. Southall and associates (1980) studied fetal cardiac rate and rhythm disturbances in 934 normal pregnancies between 30 and 40 weeks. Arrhythmias, episodes of bradycardia < 100 bpm, or tachycardia > 180 bpm were encountered in 3 percent. Most supraventricular arrhythmias are of little signiicance during labor unless there is coexistent fetal heart failure as evidenced by hydrops. Many supraventricular arrhythmias disappear in the immediate neonatal period, although some are associated with structural cardiac defects (Api, 2008). Intermittent baseline bradycardia is frequently due to congenital heart block. Conduction defects, most often complete atrioventricular (A V) block, usually are found in association with maternal connective tissue diseases (Chap. 59, p. 1142). Antepartum evaluation of the fetus with an identiied arrhythmia and potential treatment options are discussed in Chapter 16 (p. 315).


Obstentrics_Williams

Obstentrics_Williams. FIGURE 24-8 Grades of baseline fetal heart rate variability shown in the following five panels. 1. Undetectable, absent variability. 2. Minimal variability, ;5 bpm. 3. Moderate (normal) variability, 6 to 25 bpm. 4. Marked variability, >25 bpm. 5. Sinusoidal pattern. This differs from variability in that it has a smooth, sinelike pattern of regular fluctuation and is excluded in the definition of fetal heart rate variability. (Adapted with permission from National Institute of Child Health and Human Development Research Planning Workshop, 1997.) FIGURE 24-9 Internal fetal monitoring at term demonstrated occasional abrupt beat-to-beat fetal heart rate spiking due to erratic extrasystoles shown in the corresponding fetal electrocardiogram. The normal newborn was delivered spontaneously and had normal cardiac rhythm in the nursery.


Obstentrics_Williams

Obstentrics_Williams. Most fetal arrhythmias without comorbid fetal hydrops are inconsequential during labor, but they may hinder interpretation of fetal heart rate tracings. Sonographic evaluation of fetal anatomy and echo cardiography can be useful. Generally, in the absence of fetal hydrops, neonatal outcome is not measurably improved by pregnancy intervention. At Parkland Hospital, intrapartum fetal cardiac arrhythmias, especially those associated with clear amnionic fluid, are typically managed conservatively.


Obstentrics_Williams

Obstentrics_Williams. A true sinusoidal pattern such as that shown in panel 5 of Figure 24-8 can be observed with fetal intracranial hemorrhage, with severe fetal asphyxia, and with severe feral anemia. he last may stem from anti-D alloimmunization, fetomaternal hemorrhage, twin-twin transusion syndrome, fetal parvoviral infection, or vasa previa with bleeding. Insigniicant sinusoidal patterns have been reported following administration of meperidine, morphine, alphaprodine, and butorphanol (Angel, 1984; Egley, 1991; Epstein, 1982). Shown in Figure 24-10 is a sinusoidal pattern seen with maternal meperidine administration. An important characteristic of this pattern when due to narcotics is the sine frequency of 6 cycles per minute. A sinusoidal pattern also has been described with chorioamnionitis, fetal distress, and umbilical cord occlusion (lvlurphy, 1991). Young (1980a) and Johnson (1981) with their coworkers concluded that intrapartum sinusoidal fetal heart patterns were not generally associated with


Obstentrics_Williams

Obstentrics_Williams. and umbilical cord occlusion (lvlurphy, 1991). Young (1980a) and Johnson (1981) with their coworkers concluded that intrapartum sinusoidal fetal heart patterns were not generally associated with fetal compromise. hus, management is usually dictated by the clinical setting. Modanlou and Freeman (1982), based on their extensive review, proposed adoption of a strict definition: 1.


Obstentrics_Williams

Obstentrics_Williams. Stable baseline heart rate of 120 to 160 bpm with regular oscillations 2. Amplitude of 5 to 15 bpm (rarely greater) FIGURE 24-10 Sinusoidal fetal heart rate pattern associated with maternal intravenous meperidine administration. Sine waves are occurring at a rate of 6 cycles per minute. 3. Long-term variability frequency of 2 to 5 cycles per minute 4. 5. Oscillation of the sinusoidal waveform above or below a baseline 6. Absent accelerations. Although these criteria were selected to deine a sinusoidal pattern that is most likely ominous, they observed thar the pattern associated with alphaprodine is indistinguishable. Other investigators have proposed a classiication of sinusoidal heart rate patterns into mild-amplitude 5 to 15 bpm, intermediate-16 to 24 bpm, and major-::25 bpm to quantiy fetal risk (Murphy, 1991; Neesham, 1993).


Obstentrics_Williams

Obstentrics_Williams. Some have defined intrapartum sine wavelike baseline variation with periods of acceleration as pseudosinusoidal. Murphy and colleagues (1991) reported that pseudosinusoidal patterns were seen in 15 percent of monitored labors. Mild pseudosinusoidal patterns were associated with use of meperidine and epidural analgesia. Intermediate pseudosinusoidal patterns were linked to fetal sucking or transient episodes of fetal hypoxia caused by umbilical cord compression. Egley and associates (1991) reported that 4 percent of fetuses demonstrated sinusoidal patterns transiently during normal labor. hese authors observed patterns persisting for up to 90 minutes in some cases.


Obstentrics_Williams

Obstentrics_Williams. The pathophysiology of sinusoidal patterns is unclear, in part due to various deinitions. There seems to be general agreement that antepatum sine wave baseline undulations portend severe fetal anemia. Still, few anti-D alloimmunized fetuses develop this pattern (Nicolaides, 1989). The sinusoidal pattern has been reported to develop or disappear ter fetal transusion (Del Valle, 1992; Lowe, 1984). Ikeda and associates (1999) proposed that the pattern is related to waves of arterial blood pressure, reflecting oscillations in the baroreceptor-chemoreceptor feedback mechanism.


Obstentrics_Williams

Obstentrics_Williams. These refer to deviations from baseline that are temporally related to uterine contractions. Acceleration refers to a rise in fetal heart rate above baseline, and deceleration is a drop below the baseline rate. The nomenclature most commonly used in the United States is based on the timing of the deceleration in relation to contractions-thus, eary, late, or variable. he waveform of these decelerations is also significant for pattern recognition. In early and late decelerations, the slope of fetal heart rate change is gradual, resulting in a curvilinear and uniform or symmetrical waveform. With variable decelerations, the slope of fetal heart rate change is abrupt and erratic, giving the waveform a jag ged appearance. The NICHD Workshop (1997) proposed that decelerations be defined as recurrent if they accompanied �50 percent of contractions in any 20-minute period.


Obstentrics_Williams

Obstentrics_Williams. Another system now used less often to describe decelera tions is based on the pathophysiological events considered most likely to underlie the pattern. In this system, early decelera tions are termed head compression, late decelerations are termed uteroplacental insuiciency, and variable decelerations are cord compression patterns. hese are abrupt heart rate increases above the fetal heart rate baseline and defined by n onset-to-peak rise within 30 seconds (American College of Obstetricians and Gynecologists, 2017a). At 32 weeks' gestation and beyond, an acceleration has a peak � 15 bpm above baseline. Its duration is � 15 sec but <2 minutes from onset to baseline return (see Table 24-1). Before 32 weeks, a peak �10 bpm for 10 seconds to 2 minutes is considered normal. Prolonged acceleration is defined as �2 minutes but < 10 minutes.


Obstentrics_Williams

Obstentrics_Williams. According to Freeman and coworkers (2003), accelerations most often occur antepartum, in early labor, and in association with variable decelerations. Proposed mechanisms for intrapartum accelerations include fetal movement, stimulation by uterine contractions, umbilical cord occlusion, fetal stimulation during pelvic examination, scalp blood sampling, and acoustic stimulation. Accelerations are common during labor. These are virtually always reassuring and almost always conirm that the fetus is not acidemic at that time.


Obstentrics_Williams

Obstentrics_Williams. As with beat-to-beat variability, accelerations represent intact neurohormonal cardiovascular control mechanisms linked to fetal behavioral states. Krebs and colleagues (1982) analyzed electronic heart rate tracings in nearly 2000 fetuses and found sporadic accelerations during labor in 99.8 percent. Fetal heart rate accelerations during the irst or last 30 minutes during labor, or both, were a favorable sign for fetal well-being. The absence of such accelerations during labor, however, is not necessarily an unfavorable sign unless coincidental with other nonreassuring changes. he chance of acidemia in the fetus that fails to respond to stimulation in the presence of an otherwise nonreassuring pattern approximates 50 percent (Clark, 1984; Smith, 1986). his physiological response shows a gradual fetal heart rate decline and then return to baseline associated with a contraction (Fig.


Obstentrics_Williams

Obstentrics_Williams. his physiological response shows a gradual fetal heart rate decline and then return to baseline associated with a contraction (Fig. Freeman and associates (2003) defined early decelerations as those generally seen in active labor between 4 and 7 cm cervical dilation. In their deinition, the degree of deceleration is generally proportional to the contraction strength and rarely falls below 100 to 110 bpm or 20 to 30 bpm below baseline. Such decelerations are common during active labor and not associated with tachycardia, loss of variability, or other fetal heart rate changes. Importantly, early decelerations are not associated with fetal hypoxia, acidemia, or low Apgar scores. FIGURE 24-11 Features of early fetal heart rate deceleration. Characteristics include a gradual decline in the heart rate with both onset and recovery coincident with the onset and recovery of the contraction. The nadir of the deceleration is 30 seconds or more after the deceleration onset.


Obstentrics_Williams

Obstentrics_Williams. Head compression probably causes vagal nerve activation as a result of dural stimulation, and this mediates the heart rate deceleration (Paul, 1964). Ball and Parer (1992) concluded that fetal head compression is a likely cause not only of the deceleration shown in Figure 24-11 but also of those shown in Figure 24-12, which typically occur during second-stage labor. FIGURE 24-12 Two diferent fetal heart rate patterns during second-stage labor that are likely both due to head compression (upper pane0. Maternal pushing eforts (lower pane0 correspond to the spikes with uterine contractions. Fetal heart rate deceleration () is consistent with the pattern of head compression shown in Figure 24-1o1. Deceleration (B), however, is "variable" in appearance because of its jagged configuration and may alternatively represent cord occlusion.


Obstentrics_Williams

Obstentrics_Williams. FIGURE 24-13 Features of late fetal heart rate deceleration. Characteristics include gradual decline in the heart rate with the contraction nadir, and recovery occurring after the end ofthe contraction. The nadir ofthe deceleration occurs 30 seconds or more after the onset of the deceleration. Indeed, they observed that head compression is the likely cause of many variable decelerations classically attributed to cord compression.


Obstentrics_Williams

Obstentrics_Williams. The fetal heart rate response to uterine contractions can reflect uterine perfusion or placental function. A late deceleration is a smooth, gradual, symmetrical decline in fetal heart rate beginning at or after the contraction peak and returning to baseline only after the contraction has ended. his deceleration reaches its nadir within 30 seconds of its onset. In most cases, the onset, nadir, and recovery of the deceleration occur after the beginning, peak, and ending of the contraction, respectively (Fig. 24-13). The magnitude of late decelerations is seldom more than 30 to 40 bpm below baseline and typically not more than 10 to 20 bpm. Late decelerations usually are not accompanied by accelerations. Myers and associates (1973) studied monkeys in which they compromised uteroplacenral perfusion by lowering maternal aortic blood pressure. The interval or lag from the contraction onset until the late deceleration onset was directly related to basal fetal oxygenation. hey demonstrated


Obstentrics_Williams

Obstentrics_Williams. by lowering maternal aortic blood pressure. The interval or lag from the contraction onset until the late deceleration onset was directly related to basal fetal oxygenation. hey demonstrated that the length of the lag was predictive of the fetal P02 but not fetal pH. he lower the fetal P02 before contractions, the shorter the lag to the onset of late decelerations. his lag relected the time necessary for the fetal P02 to fall below a critical level necessary to stimulate arterial chemoreceptors, which mediated the decelerations.


Obstentrics_Williams

Obstentrics_Williams. Murata and coworkers (1982) also showed that a late deceleration was the irst fetal heart rate consequence ofuteroplacental-induced hypoxia. During the course of progressive hypoxia that led to death over 2 to 13 days, monkey fetuses invariably exhibited late decelerations before development of acidemia. Variability of the baseline heart rate disappeared as acidemia developed. Generally, any process that produces maternal hypotension, excessive uterine activity, or placental dysfunction can induce late decelerations. The two most common sources are hypotension from epidural analgesia and uterine hyperactivity from onset : sece: 1 ... FIGURE 24-14 Features ofvariable fetal heart rate decelerations. Characteristics include an abrupt decline in the heart rate, and onset that commonly varies with successive contractions. The deceleration measures : 15 bpm for : 15 seconds and has an onset-to-nadir phase of <30 seconds. Total duration is <2 minutes.


Obstentrics_Williams

Obstentrics_Williams. oxytocin stimulation. Maternal diseases such as hypertension, diabetes, and collagen vascular disorders can cause chronic placental dysfunction. Placental abruption can produce acute late decelerations. he most frequent deceleration patterns encountered during labor are variable decelerations attributed to umbilical cord occlusion. In a study of more than 7000 monitor tracings, variable decelerations were identified in 40 percent when labor had progressed to 5 cm dilation and in 83 percent by the end of first-stage labor (Melchior, 1985). A variable deceleration is defined as an abrupt drop in the fetal heart rate beginning with the onset of the contraction and reaching a nadir in less than 30 seconds. he decrease must last between 15 seconds and 2 minutes and must be :::15 bpm in amplitude. The onset of deceleration typically varies with successive contractions (Fig. 24-14).


Obstentrics_Williams

Obstentrics_Williams. Hon (1959) tested the efects of umbilical cord compression on fetal heart rate (Fig. 24-15). In experimental animals, complete occlusion of the umbilical cord produces abrupt, jagged-appearing deceleration of the fetal heart rate 24-16). Concomitantly, fetal aortic pressure rises. Itskovitz and colleagues (1983) observed that variable decelerations in fetal lambs occurred only after umbilical blood flow was reduced by at least 50 percent.


Obstentrics_Williams

Obstentrics_Williams. Two types ofvariable decelerations are shown in Figure 24-17. The deceleration denoted by "A" is very much like that seen with complete umbilical cord occlusion in experimental animals (see Fig. 24-16). Deceleration "B," however, has a diferent configuration because of the "shoulders" of acceleration before and ater the deceleration component. Lee and coworkers (1975) proposed that this form of variable deceleration was caused by difering degrees of partial cord occlusion. In this physiological scheme, occlusion of only the vein reduces fetal blood return, thereby triggering a baroreceptor-mediated c'Eii. 40


Obstentrics_Williams

Obstentrics_Williams. FIGURE 24-15 A. The effects oF 25-second cord compression compared with those of 40 seconds in panel (8). (Redrawn with permission from Hon EH: The fetal heart rate patterns preceding death in utero, Am J Obstet Gynecol. 1959 Jul;78(l ):47-56.) acceleration. With increasing intrauterine pressure and subsequent complete cord occlusion, fetal systemic hypertension develops due to obstruction of umbilical artery flow. This stimulates a baroreceptor-mediated deceleration. Presumably, the aftercoming shoulder of the acceleration represents the same events occurring in reverse (Fig. 24-18).


Obstentrics_Williams

Obstentrics_Williams. Ball and Parer (1992) concluded that variable decelerations are mediated vagally and that the vagal response may be due to chemoreceptor or baroreceptor activity or both. Partial or complete cord occlusion produces an increase in afterload (baroreceptor) and a drop in fetal arterial oxygen content (chemoreceptor). These both result in vagal activity leading to deceleration. In fetal monkeys, the baroreceptor relexes appear to operate during the first 15 to 20 seconds of umbilical cord occlusion followed by decline in P02 at approximately 30 seconds, which then serves as a chemoreceptor stimulus (MuellerHeubach, 1982).


Obstentrics_Williams

Obstentrics_Williams. Thus, variable decelerations represent fetal heart rate reflexes that relect either blood pressure changes due to interruption of umbilical flow or changes in oxygenation. It is likely that most fetuses have experienced brief but recurrent periods of hypoxia due to umbilical cord compression during gestation. The frequency and inevitability of cord occlusions undoubtedly have provided the fetus with these physiological mechanisms as a means of coping. The great dilemma for the obstetrician in managing variable fetal heart rate decelerations is determining when variable decelerations are pathological. According to the American College of 0bstetricians and Gynecologists (2017 a), recurrent variable decelerations with minimal-to-moderate beat-to-beat variability are indeterminate, whereas those with absent variability are abnorma.


Obstentrics_Williams

Obstentrics_Williams. FIGURE 24-16 Total umbilical cord occlusion (arrow) in the sheep fetus is accompanied by an increase in fetal aortic blood pressure. Blood pressure changes in the umbilical vessels are also shown. (Redrawn with permission from Kunzel W: Fetal heat rate alterations in partial and total cord occlusion. In Kunzel W (ed): Fetal Heart Rate Monitoring: Clinical Practice and Pathophysiology. Berlin, Springer, 1985.) FIGURE 24-17 Varying (variable) fetal heart rate decelerations. Deceleration (8) exhibits "shoulders" of acceleration compared with deceleration (A).


Obstentrics_Williams

Obstentrics_Williams. Fetal heart rate Uterine contraction occlusion Complete occlusion IIIIIIIIII I: Partial occlusion Umbilical vein Umbilical artery Fetal systolic BP Umbilical cord FIGURE 24-18 Schematic representation ofthe fetal heart rate efects with partial and complete umbilical cord occlusion. Uterine pressures generated early in a contraction cause cord compres-sion predominantly ofthe thin-walled umbilical vein. The resulting decrease in fetal cardiac output leads to an initial compensatory rise in fetal heart rate. As cord compression intensifies, umbilical arteries are then also compressed. The resulting rise in fetal systolic blood pressure leads to a vagal-mediated fetal heart rate deceleration. As the contraction abates and compression is relieved first on the umbilical arteries, elevated fetal systolic blood pressures drop and the deceleration resolves. A final increase in fetal heart rate is seen as a result of persistent umbilical vein occlusion. With completion of the uterine


Obstentrics_Williams

Obstentrics_Williams. fetal systolic blood pressures drop and the deceleration resolves. A final increase in fetal heart rate is seen as a result of persistent umbilical vein occlusion. With completion of the uterine contraction and cord compression, the fetal heart rate returns to baseline. BP = blood pressure. (Adapted with permission from Lee (V, DiLaretto pc, Lane JM: A study offetal heart rate acceleration patterns, Obstet Gynecol. 1975 Feb;45(2):142-146.) Other fetal heart rate patterns have been associatedwith umbilical cord compression. Saltatoy baseline heart rate (Fig. 24-19) was first linked o umbilical cord complications during labor (Hammacher, 1968). he pattern consists ofrapidlyrecurringcouplets of acceleration and deceleration causing relatively large oscillations of the baseline fetal heart rate. We also observed a relationship between cord occlusion and the saltatory pattern in postterm pregnancies (Leveno, 1984). In the absence of other fetal heart rate finings, these do not signal fetal


Obstentrics_Williams

Obstentrics_Williams. We also observed a relationship between cord occlusion and the saltatory pattern in postterm pregnancies (Leveno, 1984). In the absence of other fetal heart rate finings, these do not signal fetal compromise. Lamba is a pattern involving an acceleration followed by a variable deceleration with no acceleration at the end ofthe deceleration. This pattern typically is seen in early labor and is not ominous (Freeman, 2003). This lambda pattern may result from mild cord compression or stretch. Overshootis a variable deceleration followed by acceleration. The clinical significance ofthis pattern is controversial (Westgate, 2001). Prolonged Deceleration This pattern, which is shown in Figure 24-20, is deined as an isolated deceleration ::15 bpm that lasts ::2 minutes but


Obstentrics_Williams

Obstentrics_Williams. FIGURE 24-19 Saltatory baseline fetal heart rate showing rapidly recurring couplets ofacceleration combined with deceleration. < 10 minutes from onset to return to baseline. Prolonged decelerations are diicult to interpret because they are seen in many diferent clinical situations. Some of the more frequent causes are cervical examination, uterine hyperactivity, cord entanglement, and maternal supine hypotension. Epidural, spinal, or paracervical analgesia may induce a prolonged deceleration (Eberle, 1998). Hill and associates (2003) observed prolonged deceleration in 1 percent of women given epidural analgesia during labor at Parkland Hospital. Other causes of prolonged deceleration include maternal hypoperfusion or hypoxia from any cause, placental abruption, umbilical


Obstentrics_Williams

Obstentrics_Williams. FIGURE 24-20 Prolonged fetal heart rate deceleration due to uterine hyperactivity. Approximately 3 minutes of the tracing are shown, but the fetal heart rate returned to normal after uterine hypertonus resolved. Vaginal delivery later ensued. Loss of variability pH 6.9 FIGURE 24-21 Cord-compression fetal heart rate decelerations in second-stage labor associated with tachycardia and loss of variability. The umbilical cord arterial pH was 6.9. cord knots or prolapse, maternal seizures including eclampsia and epilepsy, application of a fetal scalp electrode, impending birth, or maternal Valsalva maneuver. In one example, Ambia and colleagues (2017) described prolonged decelerations lasting 2 to 10 minutes following an eclamptic seizure.


Obstentrics_Williams

Obstentrics_Williams. he placenta is efective in resuscitating the fetus if the original insult does not recur immediately. Occasionally, such self-limited prolonged decelerations are followed by loss of beat-to-beat variability, baseline tachycardia, and even a period of late decelerations, all of which resolve as the fetus recovers. Freeman and colleagues (2003) emphasize that the fetus may die during prolonged decelerations. hus, management of prolonged decelerations can be extremely tenuous. Management of isolated prolonged decelerations is based on bedside clinical judgment, which inevitably will sometimes be imperfect given the unpredictability of these decelerations.


Obstentrics_Williams

Obstentrics_Williams. Decelerations are virtually ubiquitous during the second stage of labor. In one study, only 1.4 percent of more than 7000 deliveries lacked decelerations during second-stage labor (Melchior, 1985). Both cord and fetal head compressions have been implicated as causes of decelerations and baseline bradycardia in this stage. Profound, prolonged fetal heart rate deceleration in the 10 minutes preceding vaginal delivery has been described (Boehm, 1975). And, similar prolonged second-stage decelerations were associated with a stillbirth and neonatal death (Herbert, 1981). hese experiences attest to the unpredictability of the fetal heart rate during second-stage labor.


Obstentrics_Williams

Obstentrics_Williams. Spong and associates (1998) analyzed the characteristics of second-stage variable fetal heart rate decelerations in 250 deliveries. hey found that as the total number of decelerations <70 bpm increased, the 5-minute Apgar score decreased. Of other patterns in second-stage labor, Picquard and coworkers (1988) reported that loss of beat-to-beat variability and baseline fetal heart rate < 90 bpm predicted fetal acidemia. Krebs and associates (1981) also found that persistent or progressive baseline bradycardia or baseline tachycardia was associated with lower Apgar scores. Gull and colleagues (1996) observed that abrupt fetal heart rate deceleration to < 100 bpm associated with loss of beat-to-beat variability for 4 minutes or longer was predictive of fetal acidemia. Thus, abnormal baseline heart rate-either bradycardia or tachycardia, absent beat-tobeat variability, or both-in the presence of deep second-stage decelerations is associated with a greater risk for fetal compromise (Fig.


Obstentrics_Williams

Obstentrics_Williams. With this approach, women with low-risk pregnancies are monitored for a short time on admission for labor. In one study, 3752 low-risk women in spontaneous labor at admission were randomly assigned either to auscultation of the fetal heart or to 20 minutes of electronic fetal monitoring (Mires, 2001). Use of admission electronic fetal monitoring did not improve neonatal outcome. Moreover, its use resulted in a greater number of interventions, including operative delivery. A similar study echoed these neonatal outcomes (Impey, 2003). More than half of the women enrolled in these studies eventually required continuous monitoring. A review by Devane and associates (2017) found that admission fetal monitoring programs for low-risk pregnancy are associated with a higher risk for cesarean delivery. Somewhat related, with the increasing rate of scheduled cesarean deliveries in the United States, clinicians and hospitals must decide whether fetal monitoring is required before the procedure in


Obstentrics_Williams

Obstentrics_Williams. Somewhat related, with the increasing rate of scheduled cesarean deliveries in the United States, clinicians and hospitals must decide whether fetal monitoring is required before the procedure in low-risk women.


Obstentrics_Williams

Obstentrics_Williams. Fetal heart rate pattern interpretations are subjective. hus, the potential for computer assistance to enhance the precision of identiying abnormal patterns appeared promising. he INFANT Collaborative Group (2017) studied whether the addition of computer-based decision-support software for interpretation of fetal heart rate patterns lowered the number of poor neonatal outcomes. In this trial, 23,515 women were randomized to computer-assisted interpretation compared with 23,055 women in a conventional clinical interpretation arm. Perinatal outcomes such as intrapartum stillbirth, early neonatal death, and neonatal encephalopathy were not improved by computer assistance. Cesarean delivery rates were similar in both groups. Moreover, a 2-year follow-up of a subset of the surviving children showed no diferences in their neurological development.


Obstentrics_Williams

Obstentrics_Williams. According to the American College of Obstetricians and Gynecologists (2017a), measurements of the pH in capillary scalp blood may help identiy the fetus in serious distress. However, this group also emphasizes that neither normal nor abnormal scalp pH results are predictive of neonatal outcome. Notably, the procedure is now used uncommonly and is not available at most hospitals in the United States. With sampling, an illuminated endoscope is inserted through the dilated cervix after membrane rupture and is pressed irmly against the fetal scalp (Fig. 24-22). The skin is wiped clean with a cotton swab and coated with a silicone gel, which allows fetal blood to accumulate s discrete globules. An incision is made through the fetal scalp to a depth of 2 mm with a special blade on a long handle. As a drop of blood forms on the surface, it is immediately collected into a heparinized glass capillary tube . The pH of the blood is measured promptly.


Obstentrics_Williams

Obstentrics_Williams. FIGURE 24-22 The technique of fetal scalp sampling using an amnioscope. The end of the endoscope is displaced from the fetal vertex approximately 2 cm to show the disposable blade against the fetal scalp before incision. The pH of fetal capillary scalp blood is usually lower than that of umbilical venous blood and approaches that of umbilical arterial blood. In one algorithm, 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 (Zalar, 1979). 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 conirmed. Otherwise, labor is allowed to continue, and scalp blood samples are repeated periodically.


Obstentrics_Williams

Obstentrics_Williams. he only beneits reported for scalp blood pH testing are fewer cesarean deliveries for fetal distress (Young, 1980b). However, Goodwin and coworkers (1994) showed a decrease in the scalp pH sampling rate from approximately 1.8 percent in the mid-1980s to 0.03 percent by 1992. This drop in sampling rate was not associated with a higher cesarean delivery rate for fetal distress. They concluded that scalp blood pH sampling was unnecessary. Kruger and colleagues (1999) have advocated the use of fetal scalp blood lactate concentration as an adjunct to pH. WibergItzel and associates (2008) randomly assigned 1496 fetuses to scalp blood pH analysis and 1496 to scalp blood lactate analysis. They found either to be equivalent in predicting fetal acidemia. The advantage of lactate measurement was that a smaller amount of blood was needed, which led to a lower procedural failure rate compared with scalp blood sampling for pH.


Obstentrics_Williams

Obstentrics_Williams. Clark and coworkers (1984) have suggested that fetal scalp stimulation is an alternative to scalp blood sampling. his proposal was based on the observation that heart rate acceleration in response to pinching the fetal 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. Later, Elimian and associates (1997) reported that of 58 cases in which the fetal heart rate accelerated > 10 bpm after 15 seconds of gentle digital stroking of the scalp, 100 percent had a scalp blood pH of > 7.20. Without an acceleration, however, only 30 percent had a scalp blood pH > 7.20. Following a prospective cohort study, Tahir Mahmood and coworkers (2017) concluded that fetal scalp stimulation was a reliable alternative to scalp blood pH determination.


Obstentrics_Williams

Obstentrics_Williams. Fetal heart rate acceleration in response to vibroacoustic stimulation has been recommended as a substitute for fetal scalp blood sampling (Edersheim, 1987). The technique uses an electronic artificial larynx placed approximately 1 cm from or directly onto the maternal abdomen (Chap. 17, p. 337). 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 movements (Sherer, 1994). 0 0 80 40 o ,, 15 1111111111111111111111-1-"."." ".".".".'." 45 60 75 FIGURE 24-23 Frequency distribution of umbilical artery oxygen saturation values in 1281 vigorous newborn infants. Dotted line indicates normal distribution. (Redrawn with permission from Arikan GM, Scholz HS, Petru E, et al: Cord blood oxygen saturation in vigorous infants at birth: what is normal? BJOG. 2000 Aug;l07(8):987-994.)


Obstentrics_Williams

Obstentrics_Williams. Lin and colleagues (2001) prospectively studied vibroacoustic stimulation in 113 women in labor with either moderateto-severe variable or late fetal heart rate decelerations. hey concluded that this technique is an efective predictor of fetal acidosis in the setting ofvariable decelerations. The predictability for fetal acidosis, however, is limited in the setting of late decelerations. Other investigators have reported that vibroacoustic stimulation in second-stage labor did not predict neonatal outcome or enhance labor management (Anyaegbunam, 1994).


Obstentrics_Williams

Obstentrics_Williams. Skupski and coworkers (2002) performed a metaanalysis of reports on intrapartum fetal stimulation tests published between 1966 and 2000. Four types of fetal stimulation were analyzed and included fetal scalp puncture for blood pH testing, llis clamp pinching of the fetal scalp, vibroacoustic stimulation, and digital strokingofthe fetal scalp. Results were similar for all four methods. These investigators concluded that intrapartum stimulation tests were useful to exclude fetal acidemia. They cautioned, however, that these tests are "less than perfect."


Obstentrics_Williams

Obstentrics_Williams. Using technology similar to that of adult pulse oximetry, this instrumentation allows assessment offetal oxyhemoglobin saturation once membranes are ruptured. A unique padlike sensor is inserted through the cervix and positioned against the fetal face. he transcervical device reliably registers fetal oxygen saturation in 70 to 95 percent ofwomen throughout 50 to 88 percent of their labors (Yam, 2000). Using fetal pulse oximetry, the lower limit for normal fetal oxygen saturation is generally considered to be 30 percent (Gorenberg, 2003; Stiller, 2002). However, when measured in umbilical arterial blood, fetal oxygen saturation normally varies greatly, as shown in Figure 24-23. Bloom u:


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Obstentrics_Williams. J:Jr� and associates (1999) reported that brief, transient fetal oxygen saturations <30 percent were common during labor because such values were observed in 53 percent offetuses with normal outcomes. When persistent for 2 minutes or longer, however, saturation values <30 percent were associated with a greater risk of potential fetal compromise. women with term pregnancies and in whom predeined abnor mal fetal heart rate patterns developed. Patients received either continuous fetal pulse oximetry. he use of fetal pulse oxim etrysigniicantlyreduced the cesarean delivery rate for nonreas suring fetal status from 10.2 to 4.5 percent. Alternatively, the cesarean delivery rate for dystocia rose significantly from 9 to 19 percent when pulse oximetry was used. No neonatal ben eits or adverse efects were associated with fetal pulse oximetry. Based on these observations, the Food and Drug Administra tion approved marketing of the Nellcor N-400 Fetal Oxygen Monitoring System.


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Obstentrics_Williams. Based on these observations, the Food and Drug Administra tion approved marketing of the Nellcor N-400 Fetal Oxygen Monitoring System. Since then, three other randomized trials have compared fetal pulse oximetry with standard care. In all three trials, neo natal outcomes were similar between the two study arms. East and coworkers (2006) reported that the addition of oximetry fetal heart rate pattern. However, Bloom (2006) and lauser (2005), each with their colleagues, found no diference in cesar ean delivery rates between the two study groups. Because of these indings, in 2005, the manufacturer discontinued sale of the fetal oximeter system in the United States.


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Obstentrics_Williams. As fetal hypoxia worsens, the fetal ECG changes. Namely, the mature fetus exposed to hypoxemia develops an elevated ST segment and a progressive rise in the T-wave height that can be expressed as a T:QRS ratio (Fig. 24-24). Increasing T:QRS ratios are thought to relect the fetal cardiac ability to adapt to hypoxia and appear before neurological damage. Further worsening of hypoxia then leads to progressively negative ST-segment delection that takes on a biphasic form (Fig. 24-25). It is reasonable to consider that ST-segment abnormalities might occur late in the course of fetal compromise. Indeed, it has been hypothesized that ST-segment changes relect myocardial tissue hypoxia.


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Obstentrics_Williams. Because of these indings, several investigators have assessed the value of analyzing these parameters as an adjunct to conventional fetal monitoring. The technique requires internal fetal heart monitoring and special equipment to process the fetal ECG. In 2005, the manufacturer-Neoventa Medicalreceived Food and Drug Administration approval for their ST analysis program named the STAN system. Several studies have evaluated ST-segment changes with fetal monitoring. In one randomized trial of 2400 pregnancies, neonatal outcomes were not improved compared with those in which conventional fetal monitoring alone was used (Westgate, 1993). However, the cesarean delivery rate for fetal distress declined in those with ST-segment analysis. Amer-Wahlin and colleagues (2001, 2007) found that the addition ofST-segment analysis to conventional fetal monitoring significantly lowered cesarean delivery rates for fetal distress and reduced metabolic acidemia in umbilical artery blood.


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Obstentrics_Williams. A Normal ST• Aerobic metabolism B Generation ofT:QRS ratios• Positive energy balance raw-ECG Average of 30 ECG complexes IncreasedT-wave amplitude• Hypoxia/anaerobic metabolism• Adrenaline surge R T ratio FIGURE 24-24 A. ST segment changes in normal and hypoxic conditions. B. Generation ofT:QRS ratios. (Redrawn with permission from Devoe L: ECG analysis: the next generation in electronic fetal monitoring? Contemporary Ob/Gyn, September 15,o2006.) Subsequently, Doria and associates (2007) introduced STAN as a clinical practice and reported no changes in the incidence of operative delivery or neonatal encephalopathy. And, one metaanalysis of ive randomized trials comprising 15,352 patients found that ST-segment analysis did not lower rates of cesarean delivery or fetal metabolic acidemia at birth (Becker, 2012).


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Obstentrics_Williams. Last, in a trial by the NICHD, 5532 women were randomly assigned to an ST-segment analysis arm (the open group) and 5576 to standard intrapartum management (the masked group). he primary outcome was a composite of one or more of seven events associated with fetal compromise (Belfort, 2015). In the open group, clinical practice was directed to some degree by predetermined ST-segment analysis guidelines. hese stipulated that intervention should be withheld, that is, expectant management adopted, for at least 60 minutes despite the presence of minimal variability; variable decelerations lasting �60 seconds or dropping to �60 bpm; recurrent late decelerations; or prolonged decelerations lasting >2 minutes, so long as no ST-eventwas present. hese guidelines did not pertain to the standard usual management group. Notably, in the open group, 55 women were delivered when STAN guidelines indicated that labor should continue. his composed 20 percent ofthe total 287 cesarean deliveries performed


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Obstentrics_Williams. management group. Notably, in the open group, 55 women were delivered when STAN guidelines indicated that labor should continue. his composed 20 percent ofthe total 287 cesarean deliveries performed for fetal distress in this group. Clearly, the attending physicians abandoned the open group protocol that stipulated nonintervention. They likely perceived the fetal heart rate patterns to reflect those formerly accepted in their usual practice as nonreassuring.


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Obstentrics_Williams. FIGURE 24-25 Biphasic ST-segment waveform with progressive fetal hypoxia. (Adapted with permission from Devoe L: ECG analysis: the next generation in electronic fetal monitoring? Contemporary Ob/Gyn, September 15,o2006.) The results of this trial showed that STAN had no efect on neonatal outcome or cesarean delivery rates (Belfort, 2015). In their review, Neilson and colleagues (2015) reached similar conclusions. hese results have essentially eliminated use ofSTsegment analysis in the United States, but this technology is still used in Europe. Doppler interrogation of the umbilical artery has been studied as another potential adjunct to conventional fetal monitoring. Further described in Chapter 10 (p. 213), abnormal Doppler waveforms may signiy pathological umbilical-placental vessel resistance. From their review, Farrell and associates (1999) concluded that this technique, used intrapartum, was a poor predictor of adverse perinatal outcomes.


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Obstentrics_Williams. The termetal distress is too broad and vague to be applied with any precision to clinical situations (American College ofObstetricians and Gynecologists, 2014). Uncertainty regarding the diagnosis based on interpretation of fetal heart rate patterns has given rise to descriptions such as reassuring or nonreassuring. he term "reassuring" suggests a restoration of confidence in the health of the fetus by a particular pattern. In contrast, a "nonreassuring" designation suggests inability to remove doubt. hese patterns during labor are dynamic, and they can rapidly change from reassuring to nonreassuring and vice versa. These assessments are subjective clinicaljudgments that are inevitaby subject to impeection and must be reconized as such.


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Obstentrics_Williams. These assessments are subjective clinicaljudgments that are inevitaby subject to impeection and must be reconized as such. The diiculty in assigning a nonreassuring label to fetal heart rate patterns stems in part from the fact that these patterns are more a reflection of fetal physiology than of pathology. Physiological control of heart rate includes various interconnected mechanisms that depend on blood flow and oxygenation. Moreover, the activity of these control mechanisms is inluenced by the preexisting state of fetal oxygenation, for example, as seen with chronic placental insuiciency. Importantly, the fetus is tethered by an umbilical cord, whereby blood flow is constantly in jeopardy. Moreover, normal labor is a process of increasing acidemia (Rogers, 1998). hus, normal labor is a process of repeated fetal hypoxic events that can infrequently lead to signiicant acidemia.


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Obstentrics_Williams. Identiication of "fetal distress" based on fetal heart rate patterns is imprecise and controversial. Experts in interpretation of these patterns often disagree with each other. 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. Speciically, 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.


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Obstentrics_Williams. To develop standardized and unambiguous deinitions of fetal heart rate (FHR) tracings, the NICHD (1997) held a succession of workshops in 1995 and 1996 and published recommendations for interpreting these patterns. As previously shown in Table 24-1, a second workshop was convened to reevaluate these recommendations and clariy terminology (Macones, 2008). A major result was the recommendation of a three-tier system for classification of FHR patterns (1 able 24-2). The American College of Obstetricians and Gynecologists (2017b) has recommended use of this tiered system.


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Obstentrics_Williams. A few studies have assessed this three-tiered system. J ackson and coworkers (201i1) studied 48,444 women in labor and found that category I (normal FHR) patterns were observed during labor in 99.5 percent of tracings. Category II (indeterminate FHR) patterns were found in 84.i1 percent of tracings, and category III (abnormal FHR) patterns were seen in 0.1 percent (54 women). Most-84 percent of women-had a mix of categories during labor. Cahill and colleagues (2012) retrospectively correlated the incidence of umbilical cord acidemia (pH :;7.10) with fetal heart rate characteristics during the 30 minutes preceding delivery. None of the three categories demonstrated a significant association with cord blood acidemia. The American College of Obstetricians and Gynecologists and the American Academy of Pediatrics (2014) concluded that a category I or II tracing with a 5-minute Apgar scorei> 7 or with normal arterial blood acid-base values was not consistent with an acute hypoxic-ischemic


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Obstentrics_Williams. Academy of Pediatrics (2014) concluded that a category I or II tracing with a 5-minute Apgar scorei> 7 or with normal arterial blood acid-base values was not consistent with an acute hypoxic-ischemic event.


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Obstentrics_Williams. TABLE 24-2. Three-Tier Fetal Heart Rate Interpretation System Include all of the following: • Baseline rate: 110-160 bpm Baseline FHR variability: moderate Early decelerations: present or absent Accelerations: present or absent Include all FHR tracings not categorized as Category I or III. of those encountered in clinical care. Examples include any of the following: Absence of induced accelerations after fetal stimulation Periodic or episodic decelerations Prolonged deceleration :2 min but < 1 0 min Variable decelerations with other characteristics, such as slow return to baseline, "overshoots,"


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Obstentrics_Williams. Prolonged deceleration :2 min but < 1 0 min Variable decelerations with other characteristics, such as slow return to baseline, "overshoots," Include either: • Absent baseline FHR variability and any of the following: bpm = beats per minute; FHR = fetal heart rate. Reproduced with permission from Macones GAl Hankins GO, Spong CY, et al: The 2008 National Institute of Child Health and Human Development workshop report on electronic fetal monitoring: update on definitions, interpretation, and research guidelines, Obstet Gynecol. 2008 Sep;1s12(3))661-666.


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Obstentrics_Williams. Sholapurkar (2012) challenged the validity of the threetier system because most abnormal fetal heart rate patterns fall into the indeterminate category II. It was further suggested that this resulted from most fetal heart rate decelerations being inappropriately classiied as variable decelerations due to cord compression. A group of 19 experts led by Clark (2013) observed that more than 80 percent of fetuses have FHR patterns in tier II. hey proposed a management algorithm for these fetuses, however, their hypothetical algorithm was not clinically tested.


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Obstentrics_Williams. Parer and King (2010) compared this situation in the United States with that of other countries in which a consensus on classiication and management has been reached by several professional societies. Some of these include the Royal College of Obstetricians and Gynaecologists, the Society of Obstetricians and Gynaecologists of Canada, the Royal Australian and New Zealand College of Obstetricians and Gynaecologists, and the Japan Society of Obstetrics and Gynecology. These authors further comment that the NICHD three-tier system is inadequate because category II-an indeterminate FHR pattern-contains a vast heterogenous mixture of patterns that prevents development of a management strategy.


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Obstentrics_Williams. Parer and Ikeda (2007) had previously proposed a colorcoded ive-tier system for both FHR interpretation and management. Two subsequent reports have compared the five-and three-tier systems. Bannerman and associates (2011) found that the two systems were similar in fetal heart rate interpretations for tracings that were either very normal or very abnormal. Coletta and coworkers (2012) found that the ive-tier system had better sensitivity than the three-tier system. Elliott and colleagues (2010) used computerization to measure the performance of a ive-tier classiication system but failed to successfully analyze and categorize 2472 fetal heart recordings. It is apparent that, after 50 years of continuous electronic fetal heart rate monitoring use, there is not a consensus on interpretation and management recommendations for FHR patterns (Parer, 2011). • Meconium in the Amnionic Fluid


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Obstentrics_Williams. • Meconium in the Amnionic Fluid Obstetricians have long realized that meconium during labor is problematic in the prediction of fetal distress or asphxia. Indeed, although 12 to 22 percent oflabors are complicated by meconium, only a few are linked to neonatal mortality. In an investigation from Parkland Hospital, meconium was found to be a "low-risk" obstetrical hazard because the perinatal mortality rate attributable to meconium was only 1 death per 1000 live births (Nathan, 1994).


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Obstentrics_Williams. Three theories regarding fetal passage of meconium may explain, in part, the tenuous connection between its detection and neonatal mortality. First, fetuses may pass meconium in response to hypoxia, and meconium therefore signals fetal compromise (Walker, 1953). Second, in utero passage of meconium may represent normal gastrointestinal tract maturation under neural control (Mathews, 1979). A inal theory posits that meconium passage follows vagal stimulation from common but transient umbilical cord entrapment with resultant increased bowel peristalsis (Hon, 1961).


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Obstentrics_Williams. Ramin and associates (1996) studied almost 8000 pregnancies with meconium-stained amnionic fluid delivered at Parkland Hospital. Meconium aspiration syndrome was signiicantly associated with fetal acidemia at birth. Other signiicant correlates of aspiration included cesarean delivery, forceps to expedite delivery, intrapartum heart rate abnormalities, depressed Apgar scores, and need for assisted ventilation at delivery. Analysis of the type of fetal acidemia based on umbilical blood gases suggested that the fetal compromise associated with meconium aspiration syndrome was an acute event. his is because most acidemic fetuses had abnormally increased PC02 values rather than a pure metabolic acidemia. Dawes and coworkers (1972) observed that such hypercarbia in fetal lambs induces gasping and resultant increased amnionic fluid inhalation. Jovanovic and Nguyen (1989) observed that meconium gasped into the fetal lungs caused aspiration syndrome only in asphyxiated animals.


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Obstentrics_Williams. Ramin and colleagues (1996) hypothesized that the pathophysiology of meconium aspiration syndrome includes, but is not limited to, fetal hypercarbia, which stimulates fetal respiration leading to aspiration of meconium into the alveoli. Lung parenchymal injury is secondary to acidemia-induced alveolar cell damage. In this pathophysiological scenario, meconium in amnionic fluid is a fetal environmental hazard rather than a marker of preexistent compromise. This proposed pathophysiological sequence is not all-inclusive, because it does not account for approximately half of the cases of meconium aspiration syndrome in which the fetus is not acidemic at birth.


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Obstentrics_Williams. Thus, 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. lthough normal, such meconium becomes an environmental hazard when fetal acidemia supervenes. Importantly, such acidemia occurs acutely, and therefore meconium aspiration is unpredictable and likely unpreventable. Moreover, Greenwood and colleagues (2003) showed that clear amnionic fluid was also a poor predictor. In a prospective study of 8394 women with clear amnionic fluid, they found that clear fluid was an unreliable sign of fetal wellbeing.


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Obstentrics_Williams. Growing evidence indicates that many newborns with meconium aspiration syndrome have suffered chronic hypoxia before birth (Ghidini, 2001). Blackwell and associates (2001) found that 60 percent of neonates 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 elevated fetal erythropoietin levels and increased nucleated red blood cell counts in newborns, suggest that chronic hypoxia is involved in many meconium aspiration syndrome cases (Dollberg, 2001; Jazayeri, 2000).


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Obstentrics_Williams. In the recent past, routine obstetrical management of a newborn with meconium-stained amnionic fluid included intrapartum suctioning of the oropharynx and nasopharynx. In 2005, management guidelines were signiicantly modiied. Now, the American College of Obstetricians and Gynecologists (2017c) recommends that newborns with meconium-stained amnionic fluid, regardless of their vigor, should no longer routinely receive intrapartum suctioning. Suctioning is reserved for those with airway obstruction. hey also recommend that an appropriately credentialed team with full resuscitation skills be available (Chap. 32, p. 607). TABLE 24-3. Some Resuscitative Measures for Category II or Category III Tracings Tachysystole with category II or III tracing Discontinue oxytocin or prostaglandins; tocolytics: terbutaline, magnesium sulfate


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Obstentrics_Williams. Tachysystole with category II or III tracing Discontinue oxytocin or prostaglandins; tocolytics: terbutaline, magnesium sulfate Recurrent variable decelerations Reposition mother; amnioinfusion; with cord prolapse, manually elevate Prolonged decelerations or bradycardia the presenting part while preparing for immediate delivery aSimultaneous evaluation of the suspected cause(s) is also an important step in management of abnormal FHR tracings. The combination of multiple interventions Simultaneously may be appropriate and potentially more effective than doing them individually or serially. FHR = fetal heart rate.


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Obstentrics_Williams. FHR = fetal heart rate. Principal management options for variant fetal heart rate patterns consist of correcting any fetal insult, if possible. Suggestions are listed in Table 24-3. he woman is moved to a lateral position, and supplemental oxygen is provided by mask. Correcting maternal hypotension caused by regional analgesia and discontinuing oxytocin both serve to improve uteroplacental perfusion. Vaginal examination excludes a prolapsed cord or impending delivery. Simpson and James (2005) assessed the beneits of three maneuvers in 52 women with fetal oxygen saturation sensors already in place. They used intravenous hydration-500 to 1000 mL of lactated Ringer solution given over 20 minutes; lateral versus supine positioning; and administration of supplemental oxygen at lOiLl min using a nonrebreathing mask. Each of these maneuvers signiicantly raised fetal oxygen saturation levels.


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Obstentrics_Williams. Terbutaline sulfate given to relax the uterus can be a temporizing maneuver in the management of nonreassuring fetal heart rate patterns during labor. A single 250-�g intravenous or subcutaneous injection is used to inhibit uterine contractions and thereby improve fetal oxygenation. Cook and Spinnato (1994) described their 10-year experiences with terbutaline tocolysis in 368 pregnancies. Such resuscitation improved fetal scalp blood pH values, although all fetuses underwent cesarean delivery. hese investigators concluded that although the studies were small and rarely randomized, most reported favorable results with terbutaline tocolysis for nonreassuring patterns. Small intravenous doses of nitroglycerin-60 to 180 �g-also have been reported to be beneicial (Mercier, 1997). Bullens and associates (2015) concluded in their review that tocolysis was beneicial. Still, the American College of Obstetricians and Gynecologists (20i1i7b) cites that evidence is insuicient to recommend


Obstentrics_Williams

Obstentrics_Williams. and associates (2015) concluded in their review that tocolysis was beneicial. Still, the American College of Obstetricians and Gynecologists (20i1i7b) cites that evidence is insuicient to recommend tocolysis for nonreassuring fetal heart rate patterns.


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Obstentrics_Williams. Such therapy improved the heart rate pattern in half of the women studied. Later, .Miyazaki and Nevarez (1985) randomly assigned 96 nulliparas in labor with cord compression patterns and found that those who were treated with amnioinfusion required cesarean delivery for fetal distress less often. Based on many of these early reports, transvaginal amnioinfusion has been extended into three clinical areas (Dad, 2016). hese include: (1) treatment of variable or prolonged decelerations; (2) prophylaxis for women with oligohydramnios, as with prolonged ruptured membranes; and (3) attempts to dilute or wash out thick meconium (Chap. 33, p. 620).


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Obstentrics_Williams. Many diferent amnioinusion protocols have been reported, but most provide a 500-to 800-mL bolus of warmed normal saline followed by a continuous inusion of approximately 3 mLimin (Owen, 1990; Pressman, 1996). In another study, Rinehart and colleagues (2000) gave either a 500-mL bolus of normal saline at room temperature alone or a similar bolus plus a continuous inusion at 3 mLimin. heir study included 65 women with variable decelerations, and the investigators found neither method to be superior. Wenstrom and associates (1995) surveyed use of mnioinusion in teaching hospitals in the United States. The procedure was used in 96 percent of the 186 centers surveyed, and it was estimated that 3 to 4 percent of llwomen delivered at these centers received such inusion. Potential complications of mnioinusion are summarized in Table 24-4. TABLE 24-4. Complications Associated with Amnioinfusion from a Survey of 186 Obstetrical Units Data from Wenstrom, 1995.


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Obstentrics_Williams. TABLE 24-4. Complications Associated with Amnioinfusion from a Survey of 186 Obstetrical Units Data from Wenstrom, 1995. able or prolonged decelerations attributed to cord entrapment. For variable decelerations, Hofmeyr and Lawrie (2012) reviewed the efects of amnioinfusion in the management of fetal heart rate patterns associated with umbilical cord compression. They concluded that amnioinfusion appeared to be useful in reducing the occurrence of variable decelerations, improving neonatal outcome, and lowering cesarean delivery rates. The American College of Obstetricians and Gynecologists (2016) has concluded that amnioinfusion is a reasonable approach in the treatment of repetitive variable decelerations regardless of meconium status.


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Obstentrics_Williams. For oligohydramnios, amnioinfusion has been used prophylactically to avoid intrapartum fetal heart rate patterns from cord occlusion. Nageotte and coworkers (1991) found that this resulted in signiicantly fewer and less severe variable decelerations in labor. However, the cesarean delivery rate or condition of term newborn was not improved. In a randomized investigation, Macri and colleagues (1992) studied prophylactic amnioinfusion in 170 term and postterm pregnancies complicated by both thick meconium and oligohydramnios. Amnioinfusion significantly reduced meconium aspiration syndrome rates and cesarean delivery rates for fetal distress. In contrast, Ogundipe and associates (1994) randomly assigned 116 term pregnancies with an amnionic luid index < 5 cm to receive prophylactic amnioinfusion or standard obstetrical care. Overall cesarean delivery rates, delivery rates for fetal distress, or umbilical cord acid-base studies did not difer significantly between groups.


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Obstentrics_Williams. For meconium-stained amnionic luid, Pierce and associates (2000) reviewed 13 prospective trials of intrapartum amnioinfusion for 1924 women with meconium-stained fluid. In the amnioinfusion group, newborns were signiicantly less likely to have meconium below the vocal cords, and meconium aspiration syndrome rates were lower. he cesarean delivery rate was also reduced in the amnioinfusion group. Similar results were reported by Rathore and coworkers (2002).


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Obstentrics_Williams. In contrast, several investigators were not supportive of amnioinfusion for meconium staining. For example, Usta and associates (1995) reported that amnioinfusion was not feasible in half of women with moderate or thick meconium who were randomized to this treatment. These investigators were unable to demonstrate improved neonatal outcomes with this treatment. Spong and coworkers (1994) also concluded that although prophylactic amnioinfusion did dilute meconium, it did not improve perinatal outcome. Last, Fraser and colleagues (2005) randomized amnioinfusion in 1998 women with thick meconium-stained amnionic fluid in labor and found no beneits. Hofmeyr and associates (2014) reported mixed results from their review. Because of these indings, the American College of Obstetricians and Gynecologists (2016) does not recommend amnioinfusion to dilute meconium-stained amnionic fluid.