Learning Objectives for PeriFACTS Case #680: Upon completion, the learner will be able to:
- Describe components of fetal heart rate tracing interpretation.
- Explain the biological characteristics and significance of early, variable, and late decelerations.
The clinical practice of auscultating fetal heart tones began in 1818, when Swiss surgeon Francoise Mayor reported hearing the fetal heart rate (FHR) by placing his ear against a gravid woman’s abdomen. Later, in 1888, an American named Kilian was the first to suggest that FHR information be used to identify the need for intervention for fetal distress. It was not until the 1970s, however, that recording continuous fetal heart rate and uterine activity became widely used in obstetric care. This introduction of electronic fetal monitoring (EFM) as a primary method for assessing fetal well being during labor dramatically altered obstetric practice. It is important to note that, to date, research studies have not demonstrated a significant reduction in overall perinatal morbidity or mortality with the use of continuous EFM as compared with properly performed auscultation by a skilled practitioner.
What we have gained from more than three decades of research and experience with EFM is considerable information about the nature and implications of many types of FHR changes. For example, FHR patterns that correlate closely with a favorable neonatal outcome have been identified. Likewise, FHR patterns associated with adverse neonatal outcomes also have been described. In between these two extremes, FHR patterns generate controversy. As such, the field of fetal heart rate monitoring continues to struggle with lack of uniform terminology, differing opinions in FHR interpretation, and wide variations in definition and management of nonreassuring FHR patterns.
To address these issues, the National Institute of Child Health and Human Development (NICHD) of the National Institutes of Health (NIH) convened a panel of researchers and clinicians in 1997 to examine the topic of EFM. The panel’s first recommendation was to establish a standardized set of definitions for EFM interpretation that would provide the foundation for future EFM research. The panel’s proposed standard nomenclature system for EFM interpretation then would need to be tested for validity, reliability, and reproducibility. The purpose of applying consistent EFM nomenclature when analyzing research studies and data is to improve the ability to interpret and compare studies scientifically and to be able to generalize the results of clinical trials.
Additionally, more meaningful EFM research will contribute to establishing a predictive value for EFM in the future, something that past EFM research has been unable to achieve. The ultimate goal is to be able to translate EFM research findings into evidence-based clinical practice.
In 2005, PeriFACTS adopted the NIH nomenclature for the singular purpose of encouraging obstetric nurses, nurse midwives, and obstetricians to speak the same language when discussing fetal heart rate interpretation. From feedback we have received, we are on our way toward achieving that important goal.
Systematic analysis of fetal heart rate data includes assessment of the baseline FHR, baseline FHR variability, and any periodic and/or non-periodic FHR changes, including accelerations, and early, variable, and/or late decelerations.
Baseline FHR should be judged as the average FHR rounded to increments of 5 bpm during a 10-minute segment. For many years, PeriFACTS described the FHR baseline as a range (highest and lowest) of FHR over a 10-minute segment. As of January 1, 2006, we will describe the baseline as a single number (the average as judged over a 10-minute segment) rounded to the nearest five beats to comply with AWHONN and NIH consensus panel protocols. This determination should not include periodic or episodic FHR changes or episodes of marked variability or dramatic changes in baseline. The normal FHR range is 110 bpm to 160 bpm.
Baseline FHR tachycardia is defined as a baseline FHR greater than 160 bpm persisting for at least ten minutes (again, excluding accelerations and decelerations). Baseline FHR tachycardia represents an increase in sympathetic and/or a decrease in parasympathetic autonomic nervous system tone. Baseline FHR tachycardia usually is associated with decreased baseline FHR variability. Although the baseline FHR is known to decrease as gestational age advances, the average baseline FHR difference from 28 weeks’ gestation to term is only 10 bpm. While premature fetuses may have slightly higher baseline FHRs than term fetuses, baseline fetal tachycardia seldom is attributed to prematurity alone. Baseline fetal tachycardia warrants close evaluation (see Table 1.1).
Table 1.1: Causes of Baseline FHR Tachycardia
Baseline FHR bradycardia is defined as a baseline fetal heart rate below 110 bpm for a period of at least ten minutes. It should be differentiated from a prolonged FHR deceleration, defined as a FHR decrease of at least 15 bpm that lasts longer than two minutes but less than ten minutes. Whenever baseline fetal bradycardia is suspected, the fetal heart rate must be distinguished clearly from the maternal heart rate (See Figure 1.1). Baseline fetal bradycardia most likely is the result of a persistent increase in parasympathetic (vagal) tone. As long as baseline FHR variability remains present in association with baseline bradycardia, the bradycardia can be considered benign and the tracing reassuring.
- maternal fever/infection
- maternal anxiety
- cigarette smoking
- medication or drug response, e.g.:
- parasympatholytic drugs
- beta-sympathomimetic drugs
- illicit drugs
- endogenous adrenaline/anxiety
- prolonged fetal activity/stimulation
- chronic fetal hypoxemia
- compensatory response to transient fetal hypoxemia
- fetal cardiac abnormalities
- supraventricular tachycardia
- fetal anemia
Table 1.2: Causes of Baseline FHR Bradycardia
- maternal supine positioning
- maternal hypotension
- connective tissue diseases
- prolonged maternal hypoglycemia
- maternal hypothermia
- medication or drug response, e.g.:
- umbilical cord occlusion/prolapse
- decompensating fetus
- cardiac conduction defects
- cardiac anatomic defects
- congenital heart disease
- maturity of the parasympathetic nervous system
- excessive/prolonged parasympathetic (vagal) stimulation
Baseline FHR variability is a term that is used to describe the variations in the FHR. Baseline FHR variability is a product of integrated activity between the sympathetic and parasympathetic branches of the autonomic nervous system. Baseline FHR variability, therefore, reflects the status of the central nervous system (CNS).
The NIH consensus panel decided to make no distinction between short-term variability (beat-to-beat variability) and long-term variability. Variability, therefore, is defined as fluctuations in the baseline FHR of two cycles/minute and is classified as:
- absent (no variability).
- minimal (5 bpm amplitude range).
- moderate (6 to 25 bpm amplitude range).
- marked (>25 bpm amplitude range).
The panel felt that in clinical situations, both short-term and long-term variability are taken as a unit to represent overall variability. The reader should be aware that, when needed for clinical management, short-term variability and long-term variability are recorded accurately only when a fetal scalp electrode (FSE) is being used. When external Doppler techniques (external monitoring) are used to obtain the fetal heart rate, several heartbeats are averaged (the number depends on the manufacturer of the fetal heart rate monitor).
Several of our participants have raised questions regarding the duration of the fetal sleep state in the healthy fetus. We found it necessary to clarify our position on this issue, because of the various versions that have been described by other authors. For example:
AWHONN (2003) states: Although more than 50% of the fetal sleep cycles last fewer than 40 minutes, some fetuses will have sleep cycles lasting 80 to 90 minutes or more.
Cunningham, et al. (2005) states: Sleep cyclicity has been described as varying from about 20 minutes to as much as 75 minutes. Timor-Tritsch and associates (1978)7 reported that the mean length of the quiet or inactive state for term fetuses was 23 minutes. Patrick and associates (1982)6 measured fetal body movements with real-time ultrasound for 24-hour periods in 31 normal pregnancies and found the longest period of inactivity to be 75 minutes.
Creasy, et al. (2004) states: Although state 1F (quiet sleep) and the unreactive NST seldom persist longer than 40 minutes, intervals approaching 2 hours are still most likely normal (Brown and Patrick, 19812).
Freeman, et al., (2003) states: Tests of baseline fetal status, in general, use lack of fetal activity as their endpoints. It should be appreciated that fetal sleep-like states may affect the results of nonstress tests (NSTs), fetal movement counting, and fetal respirations. Sufficient time should be allowed before interpreting these tests as nonreassuring. For NSTs and fetal movement counting, up to 60 to 80 minutes may be required before being confident that the absence of fetal reactivity and/or movement may be secondary to a fetal sleep cycle.
Because numerous opinions on this topic exist, our policy for evaluating the fetal sleep state in the healthy fetus is as follows: The normal fetus has sleep cycles that last about 20 to 40 minutes that can be interpreted as periods of decreased variability. If there are persistent patterns of decreased variability lasting longer than 40 minutes, however, further evaluation of fetal status is appropriate.
We thank you for your attention on this very important topic
- Association of Women's Health, Obstetric, and Neonatal Nurses. Feinstein N and McCartney P (2003). Fetal Heart Monitoring: Principles and Practices, (Ed. 3). Dubuque, IA: Kendall/Hunt Publishing Company, pp. 124.
- Brown R and Patrick J (1981). The nonstress test: How long is enough. American Journal of Obstetrics and Gynecology, 151, 646-651.
- Creasy RK, Resnik R, and Iams JD (2004). Maternal-Fetal Medicine: Principles and Practices, [Ed. 5]. Philadelphia, PA: W.B. Saunders, pp. 361.
- Cunningham FG, Gant NF, Leveno KJ, Gilstrap LC, Hauth JC, and Wenstrom KD (2005). Williams Obstetrics (Ed. 22). New York, NY: The McGraw-Hill Companies, Inc., pp. 374.
- Freeman RK, Garite TJ, and Nageotte MP (2003). Fetal Heart Rate Monitoring, (Ed. 3), Philadelphia, PA: Lippincott, Williams, and Wilkins, pp. 248-249.
- Patrick J, Campbell K, Carmichael L, Natale R, Richardson B (1982). Patterns of gross fetal body movements over 24-hour observation intervals during the last 10 weeks of pregnancy. American Journal of Obstetrics and Gynecology, 142, 363371.
- Timor-Tritsch IE, Dierker LJ, Hertz RH, Deagan NC and Rosen MG (1978). Studies of antepartum behavioral state in the human fetus at term. American Journal of Obstetrics and Gynecology, 132, 524-531.
Table 1.3: Causes of Decreased Baseline FHR Variability
Marked FHR variability (often referred to as saltatory) in some studies is associated with fetal hypoxia. Interventions, including the need for immediate delivery and a resuscitation team, may be warranted. This will be discussed in more detail in this month’s PeriFACTS related reading.
- medication or drug response; e.g.:
- CNS depressants
- fetal sleep cycles
- fetal CNS anomalies, e.g.:
- prolonged or severe fetal hypoxia
- cardiac anomalies
- persistent fetal tachycardia
- excessive/prolonged parasympathetic (vagal) stimulation
Fetal heart rate deceleration patterns have been given descriptive names including early, variable, and late deceleration patterns.
An early deceleration (Figure 1.2) is a gradual decrease from the FHR baseline with a nadir in 30 seconds that then returns to baseline, associated with a uterine contraction. The early deceleration occurs simultaneously with the uterine contraction in a mirror-image fashion.
Although the exact mechanism of early decelerations has not been proved, compression of the fetal head during contractions is believed to precipitate a reflex vagal response, resulting in a slowing of the FHR. Early decelerations occur simultaneously with contractions, and the nadir (lowest point) of the decelerations coincides with the acme or peak of the contractions, when pressure on the fetal head is the greatest. Early decelerations rarely decrease more than 20 bpm below the baseline FHR and, therefore, often are described as shallow decelerations. Early decelerations are uniform in appearance; i.e., they look similar to one another in shape, except that stronger contractions often result in deeper early decelerations.
FHR variability usually is moderate in association with a pattern of early decelerations. Although it would seem that fetal head compression must occur in virtually all labors, in fact, classic early decelerations clinically are uncommon.
Figure 1.2: Early Decelerations
Early decelerations are associated with:
- early active stage of labor (4 to 7 cm).
- a higher incidence of cephalopelvic disproportion (CPD).
- persistent posterior presentation.
- normal fetal oxygenation.
INTERPRETATION AND INTERVENTIONS FOR EARLY DECELERATIONS
Early decelerations are a normal reflex response to increased pressure on the fetal head. Early decelerations are not associated with fetal hypoxia, acidosis, or adverse perinatal outcomes and, therefore, require no intervention. It is important, however, to differentiate between a pattern of early decelerations and a pattern of late decelerations, because the characteristics of both are similar, while their clinical significance is very different. An accurate assessment or recording of uterine contractions is essential in distinguishing between a pattern of early versus late decelerations. Also, early decelerations usually are accompanied by normal baseline variability, whereas late decelerations frequently are accompanied by decreased baseline FHR variability.
A variable deceleration (Figure 1.3) is an abrupt decrease (nadir <30 seconds) in FHR lasting <10 minutes from onset to return to baseline. If the deceleration exceeds ten minutes, it is a baseline change (normal, tachycardia, or bradycardia).
Figure 1.3: Variable Decelerations
Classic variable decelerations demonstrate an initial brief acceleration (primary “shoulder” acceleration or anterior “shoulder”), followed by an abrupt, precipitous fall from the baseline that recovers back to baseline as abruptly as it fell. This recovery then is followed by a second, brief acceleration (secondary acceleration or posterior “shoulder”). Classic variable decelerations are jagged and irregularly shaped, often appearing spiked or U-, V-, or W-shaped. Baseline FHR variability normally is maintained with a pattern of classic variable decelerations. Classic variable decelerations vary significantly, and no two are exactly alike. They can occur before, during, or after contractions.
Variable decelerations result from compression of the umbilical cord. The umbilical cord consists of two small, thick-walled arteries and one large, thin-walled vein. The arteries transport deoxygenated blood and waste products away from the fetus back to the placenta. The vein transports oxygenated blood and nutrients from the placenta into the fetal circulation. When umbilical cord perfusion is decreased due to mechanical compression, the thin-walled vein becomes occluded first. Blood no longer can return from the placenta to the fetal circulation but still can exit the fetus via the unimpeded umbilical arteries. The decreased venous return to the heart precipitates a transient reflex tachycardia that is seen as the initial, anterior shoulder in the classic variable deceleration. If the pressure on the cord becomes greater, the small, thick-walled umbilical arteries also become compressed. The result of this arterial compression is a rapid increase in fetal blood pressure that activates a fetal baroreceptor-reflex response. Vagal stimulation occurs, and the FHR decreases abruptly. Once compression of the umbilical cord is relieved, the higher elastic arteries open first, but the umbilical vein still may be compressed. A transient tachycardia (posterior shoulder) may occur. As perfusion in the umbilical vein resumes, the blood pressure normalizes and the FHR returns to baseline.
Variable decelerations are the most common pattern observed during labor. Transiently reduced umbilical cord perfusion generally is well tolerated by healthy fetuses. If, however, a fetus’s oxygen reserves are borderline because of a disease process, or if reduced umbilical cord perfusion is persistent and prolonged enough, fetal PCO2 levels rise and respiratory acidosis initially and metabolic acidosis later can occur.
Factors that are associated with variable decelerations:
- short umbilical cord.
- nuchal cord.
- cord malposition or body entanglement.
- occult or obvious prolapsed cord.
- rapid descent of the fetus.
- decreased amniotic fluid volume.
- knot in the cord.
- decreased Wharton’s jelly.
Do you have questions that your doctors or nurses have asked that you would like us to try to answer? Remember, these answers would be just our editorial opinion and are not to be used in the legal defense of a case or for active patient management.
Questions you astute readers have asked in the past.
- Why doesn’t a variable deceleration go below 55 to 60 bpm?
ANSWER: When the fetal parasympathetic nervous system is activated fully by cord compression of the umbilical arteries, it drops the fetal heart rate to what would be equivalent to a complete heart block with the recorded heart rate being the ventricular rate. If the fetal heart rate is below 55 to 60 bpm, think hypoxia!
- The decelerations in a variable deceleration are very abrupt with steep slopes while a late deceleration is more gradual, yet both work through the parasympathetic system of the fetus. What causes the difference?
ANSWER: The easiest way to differentiate the two patterns is to imagine the changes in fetal blood pressure that cause the reflex heart rate decrease. When the umbilical arteries are compressed, there is a rapid rise in blood pressure, resulting in a rapid fall in heart rate. In a late deceleration, hypoxemia during a uterine contraction produces a more gradual increase in blood pressure. This is accompanied by a more gradual decrease and then slower recovery of the heart rate.
USE OF THE TERMS "REASSURING" AND "NONREASSURING"
The 1997 National Institutes of Health (NIH) Consensus Panel on Fetal Monitoring Interpretation chose not to include the terms reassuring and nonreassuring in their vocabulary. Nonetheless, these terms are used so frequently in clinical practice that PeriFACTS has chosen to use them in the interpretation of fetal heart rate (FHR).
Keep in mind that the characteristics of the FHR tracing include determining the baseline FHR, degree of variability, presence or absence of accelerations, and presence or absence of decelerations. These determinations must be made in relationship to the fetus's gestational age. The terms reassuring and nonreassuring will be applied to FHR interpretation as follows:
REASSURING: This term describes a FHR tracing whose characteristics indicate an adequately oxygenated fetus, thus allowing the fetus to remain in-utero. In essence, a reassuring fetal heart rate tracing allows management of the pregnancy to continue without additional or more intensive fetal monitoring, or the need to consider delivery.
NONREASSURING: This term is the opposite of reassuring and requires that if the pregnancy is to continue, then more intensive fetal monitoring must be carried out, or the fetus must be delivered.
Several attempts have been made to classify variable decelerations’ severity on the basis of depth and duration. The actual clinical use of these classifications is questionable. The nonreassuring, variable deceleration does, however, deserve further discussion (Figure 1.4). Krebs et al. examined the frequency and significance of various features of variable decelerations and identified characteristics associated with a higher incidence of fetal hypoxemia (Krebs, et al., 1983).
Nonreassuring variable decelerations classically have no anterior or posterior shoulder and tend to “slide” into a deceleration in a somewhat sluggish manner.
The feature of nonreassuring variable decelerations that most significantly indicates fetal hypoxemia, however, is loss of variability within the variable decelerations. Nonreassuring variable decelerations exhibit:
- prolonged or gradual return to baseline FHR.
- presence of repetitive overshoots (a compensatory acceleration of at least 20 bpm lasting 20 seconds that only follows the deceleration).
- rising baseline FHR.
- absence or loss of baseline variability.
- development of tachycardia.
- persistent decelerations in conjunction with nadirs <70 bpm and durations >60 seconds.
Figure 1.4: Nonreassuring Variable Decelerations
- continued close assessment for classic versus atypical features, as well as baseline FHR and variability changes.
- maternal repositioning to maximize cord perfusion.
- intravenous bolus hydration with a volume expander (e.g., lactated Ringer’s) to promote maternal cardiac output, uterine perfusion, and fetal oxygen availability.
- amnioinfusion to provide buoyancy and cushioning for the cord.
- oxygen by facemask at 10 L/min, if persistent atypical features or changes in baseline rate or variability occur.
- cervical examination to assess for cord prolapse and labor progress.
- assessment of fetal capillary blood gas status, if feasible.
- plans for delivery by the most expeditious route, if the pattern persists despite the above interventions.
Late decelerations (Figure 1.5) are shallow, uniform-shaped decelerations that are characterized by a gradual decrease from and return to the baseline fetal heart rate. The nadir of late decelerations usually is between 5 to 30 bpm below the baseline, rarely more than 30 bpm. Late decelerations typically begin near the acme of contractions, with return to baseline FHR always occurring after the contractions have ended. Late decelerations must demonstrate both this characteristic shape (i.e., shallow, uniform shape with a gradual onset and recovery) and timing (i.e., beginning after the contractions begin and ending after the contractions end).
Figure 1.5: Late Decelerations
Oxygenated blood reaches the uterus via the maternal uterine arteries. The uterine arteries branch into numerous smaller arteries which traverse the uterine muscle (myometrium) becoming spiral arterioles that empty maternal oxygen- and nutrient-rich blood into the intervillous spaces within the placenta. Within the intravillous spaces, transfer of oxygen and nutrients into the fetal circulation occurs. Fetal blood vessels within villi of the placenta extend into these intervillous spaces. Maternal blood from the spiral arterioles bathes these fetal blood vessels. Normally, maternal blood does not mix with fetal blood, but rather, it is separated by vascular membranes across which oxygen and nutrients are transported via mechanisms of simple diffusion, facilitated transport, and active transport.
Uterine contractions result in compression of the maternal spiral arterioles that traverse the uterine muscle. During the contraction, less oxygen-rich maternal blood is available in the intervillous spaces for oxygen transfer into the fetal circulation. This decrease in placental perfusion results in a decline in maternal-fetal oxygen transfer and a decrease in fetal PO2. When fetal PO2 falls below a minimal normal threshold, chemoreceptors located in the fetal aorta and carotid arteries detect this decreased PO2 and activate the parasympathetic nervous system via the vagus nerve. The vagus nerve is a cranial nerve that innervates the sinoatrial (S-A) and atrioventricular (A-V) nodes, the pacemakers that control heart rate. Vagal stimulation to these pacemakers results in a slowing of the fetal heart rate. Since the fall in fetal PO2 occurs after the contraction is well established, the decrease in FHR also occurs well after the contraction has begun. It takes some time for the reduced uteroplacental oxygen transfer to decrease fetal PO2 levels sufficiently to trigger a response. This time is referred to as “lag” time, and it accounts for the delay in onset of a late deceleration until after the contraction is well established. Likewise, when uteroplacental oxygen transfer becomes optimal again, it takes some seconds before fetal blood PO2 returns to normal, accounting for the delay in FHR return to baseline until well after the contraction is over.
Changes in the fetal blood pressure offer the second theory to explain the mechanism of late decelerations. During a uterine contraction, as less oxygen is available in the intervillous space, the compromised fetus may respond by releasing norepinephrine and epinephrine. These catecholamines, in turn, would produce a rise in the fetal blood pressure which, in turn, would produce a reflex bradycardia.
A different type of late deceleration occurs when a fetus already has sustained hypoxia significant enough to shift to anaerobic metabolism and lactic acid buildup. In this case, severe fetal hypoxia and acidosis act to depress the fetal myocardium directly and may result in late decelerations that begin even closer to the onset of contractions. Also, the acidosis may depress the fetal heart so significantly that it becomes barely able to respond to further changes in parasympathetic signals. These shallow, late decelerations may be subtle and may reflect a blunted or decompensatory response to significant fetal hypoxia and metabolic acidosis. Although the depth of late decelerations normally varies with the intensity of contractions, the depth is not indicative of the significance of fetal hypoxia, and ominous, late decelerations may be so shallow (e.g., 5 bpm change from baseline) that they are overlooked. These subtle, late decelerations usually are accompanied by absent baseline FHR variability and may be indicative of a fetus near death.
Uteroplacental insufficiency is the term that is used to describe the situation when maternal-fetal oxygen transfer becomes insufficient to meet fetal oxygen requirements. A healthy fetus normally has enough oxygen reserve (i.e., tissue oxygen levels that are well above the minimal oxygen levels required for normal cellular function) so that small or brief decreases in PO2 accompanying contractions of normal labor are tolerated easily and tissue oxygen levels in the fetus remain within normal limits. When fetal oxygen reserve is borderline, the transient decreases in PO2 that occur with normal labor contractions may reduce fetal oxygen concentration below threshold, triggering a compensatory response.
Late decelerations are associated with:
- maternal hypotension from supine positioning, trauma, hemorrhage, or epidural or spinal anesthesia.
- maternal chronic or pregnancy-induced hypertension.
- maternal collagen vascular disease.
- maternal diabetes mellitus.
- uterine hyperstimulation from oxytocin or prostaglandin.
- maternal cardiovascular disease.
- placental postmaturity.
- illicit drug use (e.g., cocaine, amphetamines, etc.).
- abruptio placentae.
- placental malformation.
A sustained pattern of late decelerations potentially is ominous.
Transient events may occur that produce a brief pattern of late decelerations (e.g., maternal hypotension from an epidural anesthetic). These patterns are more amenable to treatment and resolution than the late deceleration associated with severe hypoxia and acidosis.
Precipitating factors that are associated with development of reversible late decelerations:
- maternal hypotension from:
- supine positioning.
- regional anesthesia.
- decreased maternal arterial hemoglobin/oxygen saturation from:
Interventions for a pattern of late decelerations include:
- assessment and treatment of possible causes, such as maternal hypotension following epidural anesthesia.
- close observation of accompanying baseline FHR and baseline variability.
- maternal lateral repositioning to promote cardiac output and uterine blood flow.
- intravenous bolus hydration with a volume expander (e.g., lactated Ringer’s) to enhance maternal intravascular volume and to promote uterine blood flow.
- maternal oxygen administration via facemask at 10 L/min, to maximize maternal-fetal oxygen pressure gradients and to facilitate oxygen transfer to the fetus.
- discontinuing any oxytocin infusion and/or administering a rapid-acting tocolytic such as terbutaline to decrease uterine activity. (This also enhances maternal cardiac output.)
- fetal scalp capillary blood gas assessment, if feasible.
- preparations for delivery by the most expeditious route, if the pattern persists.
Despite controversy and debate, fetal heart rate interpretation remains a mainstay of obstetric care and poor interpretation a leading cause of medical malpractice suits. Understanding the physiology and varying patterns of fetal heart rate tracings promotes improved obstetric care and reduces malpractice liability exposure.
- Krebs HB, Petres RE, and Dunn LJ (1983). Intrapartum fetal heart rate monitoring: VIII. Atypical variable decelerations. American Journal of Obstetrics and Gynecology,145(3), 297-305.
- The National Institute of Child Health and Human Development Research Planning Workshop (1997). Electronic fetal heart rate monitoring: Research guidelines for interpretation. Journal of Obstetric, Gynecologic, and Neonatal Nursing, 26, 635-640.
- Woods JR, Glantz CJ, Pittinaro DR, and Giffi, C (2007). PeriFACTS’s Principles of Fetal Heart Rate Monitoring. Rochester, NY: University of Rochester.