CME/CE

JANUARY 2008

Intrapartum FHR Monitoring: The Evolution of Consensus

David A. Miller, MD

Continuing Medical Education

GOAL To promote the use of standardized terminology, interpretation, and management for electronic fetal heart rate (FHR) monitoring in women. OBJECTIVES To define FHR terminology and interpretation based on consensus statements from leading agencies and organizations. To explore the physiology behind changes in FHR and the implications for fetal well-being, especially with regard to neurologic damage. To discuss the status of FHR-based management strategies. ACCREDITATION This activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of Albert Einstein College of Medicine and Quadrant HealthCom Inc. Albert Einstein College of Medicine is accredited by the ACCME to provide continuing medical education for physicians. This activity has been peer reviewed and approved by Brian Cohen, MD, Professor of Clinical ObGyn, Albert Einstein College of Medicine. Review date: December 2007. It is designed for ­ObGyns, primary care physicians, and nurse practitioners. Albert Einstein College of Medicine designates this educational activity for a maximum of 1 AMA PRA Category 1 Credit™. Physicians should only claim credit commensurate with the extent of their participation in the activity. Participants who answer 70% or more of the questions correctly will obtain credit. To earn credit, see the instructions on page 65 and mail your answers according to the instructions on page 66. CONFLICT OF INTEREST STATEMENT The “Conflict of Interest Disclosure Policy” of Albert Einstein College of Medicine requires that authors participating in any CME activity disclose to the audience any relationship(s) with a pharmaceutical or equipment company. Any author whose disclosed relationships prove to create a conflict of interest, with regard to their contribution to the activity, will not be permitted to present. The Albert Einstein College of Medicine also requires that faculty participating in any CME activity disclose to the audience when discussing any unlabeled or investigational use of any commercial product, or device, not yet approved for use in the United States. Dr Miller reports no conflict of interest. Dr Cohen reports no conflict of interest.

In the United States today, intrapartum fetal heart rate (FHR) monitoring is the most common obstetric procedure, used in more than 3.4 million deliveries and impacting nearly 7 million mothers and fetuses annually.1 Although its clinical value remains a source of debate and controversy, intrapartum FHR monitoring is a practical reality. It requires a level of multidisciplinary communication, coordination, and shared responsibility that is unique in the field of medicine, and the stakes can be very high. Although it is now apparent that most cases of neurologic injury do not originate in the intrapartum period,2 a significant minority may be related to intrapartum events, and preventing such injuries must be a top priority.

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FHR MONITORING AND PERINATAL INJURY

In July 2004, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) addressed the issue of preventable perinatal injury, identifying poor communication of abnormal FHR patterns as a leading risk factor.3 The Commission recommended that health care organizations promote the use of standardized terminology to communicate abnormal FHR tracings, and develop clear guidelines for FHR interpretation. Unfortunately, in 2004, broad consensus regarding standardized FHR terminology had yet to be established.

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FHR TERMINOLOGY—ACHIEVING CONSENSUS

In 1997, the National Institute of Child Health and Human Development (NICHD) published recommendations for standardized definitions of FHR patterns.4 Recently, these recommendations have been endorsed by ACOG,1 the Association of Women’s Health, Obstetric and Neonatal Nurses (AWHONN), and the American College of Nurse Midwives (ACNM), reflecting unprecedented multidisciplinary consensus regarding standardized FHR terminology. The definitions proposed by the NICHD are summarized in Table 1. For detailed review, readers are encouraged to refer to the 1997 NICHD publication4 and to the 2005 ACOG Practice Bulletin # 70.1

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TABLE 1. Definitions of FHR patterns

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FHR INTERPRETATION—EVOLVING CONSENSUS

The objective of intrapartum FHR monitoring is to prevent fetal injury that might result from disruption of normal fetal oxygenation during labor. Fetal oxygenation involves the transfer of oxygen from the external environment to the fetus and the subsequent fetal response. En route from the environment to the fetus, oxygen is carried by maternal and fetal blood along the “oxygen pathway” that includes the maternal lungs, heart, vasculature, uterus, placenta and umbilical cord (Figure 1). Disruption of oxygen transfer can occur at any or all of these points and, if recurrent or sustained, can lead to a cascade of fetal physiologic changes, including: hypoxemia, hypoxia, metabolic acidosis, metabolic acidemia, failure of peripheral vascular smooth muscle contraction, hypotension and potential injury (Figure 1). Evidence-based FHR interpretation can provide reliable information regarding several key aspects of fetal oxygenation.

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FIGURE 1. With respect to fetal oxygenation, practical intrapartum FHR interpretation can be distilled into three central concepts. Courtesy of David A. Miller, MD

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VARIABLE DECELERATION

A variable deceleration is defined as an abrupt decrease in FHR at least 15 beats per minute (bpm) below the baseline lasting at least 15 seconds and less than 2 minutes.1 The underlying cause is compression of the umbilical arteries within the umbilical cord, resulting in an abrupt increase in fetal blood pressure and an abrupt baroreceptor-mediated reflex slowing of the FHR.7 When cord compression is relieved, autonomic reflexes subside and the FHR returns to baseline. At times, clinically benign early decelerations caused by fetal head compression may mimic the appearance of variable decelerations.7 However, unless the distinction can be made with certainty, a variable deceleration should be attributed to disruption of the “oxygen pathway” at the level of the umbilical cord.

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LATE DECELERATION

Late deceleration of the FHR is defined as a gradual decrease in FHR from the baseline associated with a uterine contraction. In most cases the onset, nadir, and recovery of the deceleration occur after the beginning, peak, and end of the contraction, respectively.1 A late deceleration is a reflex fetal response to transient disruption of fetal oxygenation during a uterine contraction.8 Myometrial contractions compress uterine blood vessels and can disrupt maternal perfusion of the placenta. Reduced delivery of oxygenated maternal blood to the intervillous space can reduce the diffusion of oxygen into fetal blood, leading to transient fetal hypoxemia. Subsequent chemoreceptor stimulation triggers reflex sympathetic outflow, peripheral vasocon-striction and centralization of blood volume, favoring perfusion of the brain, heart, and adrenal glands. The consequent rise in blood pressure triggers a baroreceptor-mediated reflex slowing of the FHR.8 When the contraction ends and maternal perfusion of the intervillous space is reestablished, autonomic reflexes subside and the FHR returns to baseline. Although commonly attributed to “uteroplacental insufficiency,” late decelerations can result from disruption of oxygen transfer at any point along the pathway from the environment to the fetus. If recurrent disruption of fetal oxygenation progresses to the stage of metabolic acidemia, a late deceleration may result from direct hypoxic myocardial depression.10 In that event, other FHR abnormalities would be anticipated, such as minimal-absent variability and absent accelerations.

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PROLONGED DECELERATION

A prolonged deceleration is defined as a decrease in FHR at least 15 bpm below the baseline lasting at least 2 minutes but less than 10 minutes. The deceleration reflects disrupted oxygen transfer from the environment to the fetus at one or more points along the oxygen pathway. When the disruption is caused by mechanical compression of the umbilical cord, a prolonged deceleration begins as a baroreceptor-mediated reflex response to an abrupt rise in fetal blood pressure. When disruption of oxygen transfer is due to an acute event such placental abruption or uterine rupture causing an abrupt drop in fetal Po2, the deceleration involves reflex peripheral vasoconstriction, centralization of blood volume, increased blood pressure, and baroreceptor-mediated slowing of the FHR.10 Sustained disruption of fetal oxygenation can lead to metabolic acidemia, hypotension, and direct hypoxic myocardial depression.10 It is likely that both mechanisms (autonomic reflex and direct myocardial depression) contribute to the pathophysiology of a prolonged deceleration, however their precise relative roles are not known. In general, autonomic reflexes appear to predominate initially and direct hypoxic myocardial depression appears to occur late in the process.

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FETAL RESPONSE TO DISRUPTED OXYGEN TRANSFER

As discussed above, all clinically significant FHR decelerations (variable, late, prolonged) have one thing in common. They all reflect disruption of the “oxygen pathway” from the environment to the fetus. Intermitted episodes of disrupted oxygenation are common in the course of normal labor. However, recurrent or sustained disruption of oxygen transfer can culminate, eventually, in metabolic acidemia, hypotension, and potential injury (Figure 1).

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THE INJURY THRESHOLD

In 1999, the International Cerebral Palsy Task Force published a consensus statement regarding the relationship between intrapartum events and neurologic injury that was supported by ACOG and similar organizations from Australia, New Zealand, and Canada.5 In 2003, the ACOG Task Force on Cerebral Palsy and the American Academy of Pediatrics (AAP) released a comprehensive review of the medical literature regarding intrapartum neurologic injury, likewise receiving widespread support.6 These landmark publications documented broad consensus regarding the critical link between intrapartum disruption of fetal oxygenation and subsequent neurologic injury. Specifically, both groups identified significant metabolic acidemia (umbilical artery pH <7.0 and a buffer base deficit ≥12 mmol/L) as an essential pre-condition to neurologic injury caused by intrapartum disruption of fetal oxygenation. The importance of this consensus position is underscored by the recognition that two FHR characteristics, moderate variability and accelerations, provide reliable information regarding the absence of metabolic acidemia and, by extension, the absence of intrapartum hypoxic injury.

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MODERATE VARIABILITY

Baseline FHR variability is defined in Table 1. Moderate variability is defined by an amplitude range of 6-25 bpm. Many factors interact to regulate fetal cardiac output on a moment-to-moment basis, causing variability in the FHR. Fluctuations in fetal Po2, Pco2 and blood pressure, detected by chemoreceptors and baroreceptors, trigger sympathetic and parasympathetic responses that modulate fetal cardiac output in order to optimize the distribution of oxygenated blood. Moderate FHR variability indicates that this process is functioning normally, and is highly predictive of the absence of metabolic acidemia at the time it is observed.9-12

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ACCELERATION

The definition of FHR acceleration is summarized in Table 1. Accelerations occur in association with fetal movement, probably involving peripheral proprioceptor stimulation, circulating catecholamines and fluctuating autonomic input. There is extensive evidence that FHR accelerations are highly predictive of the absence of fetal metabolic acidemia at the time they are observed.12,13

In summary, with respect to fetal oxygenation, practical intrapartum FHR interpretation can be distilled into three central concepts, as illustrated in Figure 1.

1. All clinically significant FHR decelerations (variable, late, prolonged) reflect disruption of oxygen transfer from the environment to the fetus at one or more points along the oxygen pathway.7,8
2. Disruption of oxygen transfer from the environment to the fetus does not result in neurologic injury (cerebral palsy) unless the fetal response progresses at least to the stage of signi-ficant metabolic acidemia (umbilical artery pH <7.0 and base deficit ≥12 mmol/L).5,6
3. Moderate FHR variability and accelerations are highly predictive of the absence of metabolic acidemia at the time they are observed.9-13

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CONCLUSION

Significant progress has been made toward consensus in FHR monitoring terminology and interpretation. The next critical step is a standardized approach to the decision-making process underlying the management of intrapartum FHR tracings. The ideal management decision model will be practical, evidence-based, consensus-driven, teachable, and testable.

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David A. Miller, MD, is Professor of Clinical Obstetrics, Gynecology, and Pediatrics, Keck School of Medicine, University of Southern California; and Medical Director, CHLA-USC Institute for Maternal Fetal Health, USC Perinatal Group, Los Angeles, Calif.

References

1. Intrapartum fetal heart rate monitoring. ACOG Practice Bulletin No.70. American College of Obstetricians and Gynecologists. Obstet Gynecol 2005;106:1453-1461.
2. Paneth, N. The causes of cerebral palsy. Recent evidence. Clin Invest Med. 1993;16:95-102.
3. Joint Commission on Accreditation of Healthcare Organizations, Sentinel even # 30, July, 2004.
4. Electronic fetal heart rate monitoring: research guidelines for interpretation. National Institute of Child Health and Human Development Research Planning Workshop. Am J Obstet Gynecol. 1997; 177:1385-1390.
5. MacLennan A. A template for defining a causal relation between acute intrapartum events and cerebral palsy: International consensus statement. BMJ. 1999;319:1054-1059.
6. American College of Obstetricians and Gynecologists’ Task Force on Neonatal Encephalopathy and Cerebral Palsy, American College of Obstetricians and Gynecologists, American Academy of Pediatrics. Neonatal encephalo-pathy and cerebral palsy: Defining the patho-genesis and pathophysiology. Washington: American College of Obste-tricians and Gynecologists, 2003.
7. Ball RH, Parer JT. The physiologic mechanisms of variable decelerations. Am J Obstet Gynecol. 1992;166:1683-1688.
8. Martin CB Jr, de Haan J, van der Wildt B, Jongsma HW, Dieleman A, Arts TH. Mechanisms of late decelerations in the fetal heart rate. A study with autonomic blocking agents in fetal lambs. Eur J Obstet Gynecol Reprod Biol. 1979;9(6): 361-373.
9. Parer JT, King T, Flanders S, Fox M, Kilpatrick SJ. Fetal acidemia and electronic fetal heart rate patterns. Is there evidence of an association. J Matern Fetal Neonatal Med. 2006;19: 289-294.
10. Low JA, Victory R, Derrick EJ. Predictive value of electronic fetal monitoring for intrapartum asphyxia with metabolic acidosis. Obstet Gynecol. 1999;93:285-291.
11. Williams KP, Galerneau F. Intrapartum fetal heart rate patterns in the prediction of neonatal acidemia. Am J Obstet Gynecol. 2003;188:820-823.
12. Elimian A, Figueroa R, Tejani N. Intrapartum assessment of fetal well-being: a comparison of scalp stimulation with scalp blood pH sampling. Obstet Gynecol. 1997;89:373-376.
13. Skupski DW, Rosenberg CR, Eglington GS. Intrapartum fetal stimulation tests: a meta-analysis. Obstet Gynecol. 2002;99:129-134.

DISCLAIMER

The opinions expressed herein are those of the author and do not necessarily represent the views of the sponsor or the publisher. Please review complete prescribing information of specific drugs or combination of drugs, including indications, contraindications, warnings and adverse effects before administering pharmacologic therapy to patients.

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