Direct Fetal Heart Rate and Uterine Activity Monitoring

Direct FHR monitoring involves transcervical application of an ECG electrode to the fetus, dilation of the cervix, rupture of the membranes, and access to the fetal presenting part. These requirements limit the use of direct monitoring to the intrapartum period. The bipolar fetal ECG electrode is attached directly to the fetal presenting part by gently screwing a small spiral metal wire into the skin. When one pole of the electrode is applied to the fetal presenting part and the other pole is bathed in vaginal fluid to complete the electrical circuit, the ECG electrode detects electrical impulses that originate in the fetal heart; amplified signals are processed by a cardiotachometer ( Fig. 15-1 ). Computer logic compares each incoming fetal QRS complex with the one immediately preceding it. The time interval between the two complexes is measured electronically and is used to calculate a heart rate, which is plotted as a point on the FHR graph located on the upper channel of the paper chart. This process is repeated with each cardiac cycle to produce a series of closely spaced individual points that appear on the paper chart as an irregular line that represents a graphic instantaneous display of the FHR.

Techniques used for direct monitoring of fetal heart rate (FHR) and uterine contractions (UC). The fetal electrocardiogram is obtained by direct application of the scalp electrode, which is then attached to a leg plate on the mother’s thigh. The signal is transmitted to the monitor, where it is amplified, counted by the cardiotachometer, and then recorded. Uterine contractions are assessed with an intrauterine pressure catheter connected to a pressure transducer. This signal is then amplified and recorded.

Direct assessment of uterine activity uses a thin, flexible intrauterine pressure catheter (IUPC) placed transcervically into the amniotic cavity. Intrauterine pressure is transmitted from the amniotic fluid through the fluid-filled catheter to an external pressure transducer. The transducer converts pressure measurements into electrical signals to permit the continuous display of pressure readings on the uterine activity graph located on the lower channel of the paper chart. Newer catheters use closed systems with a strain gauge or sensors in the catheter tip that relay signals to a strain gauge located at the base of the catheter. A second port can be used to infuse saline into the amniotic cavity ( amnioinfusion ) to relieve variable FHR decelerations caused by umbilical cord compression. An appropriately calibrated IUPC permits accurate assessment of the frequency, duration, and intensity of uterine contractions as well as the baseline uterine tone between contractions .

Indirect Fetal Heart Rate and Uterine Activity Monitoring

Indirect (external) monitoring does not require the transcervical placement of electrodes or catheters. Consequently, external FHR monitoring uses an ultrasound transducer applied with straps to the maternal abdomen and can be performed prior to labor. Ultrasound waves produced by the transducer are transmitted to the maternal skin through coupling gel; these waves penetrate maternal and fetal tissues and are reflected by moving tissue interfaces. Waves reflected from moving structures of the fetal heart return to the transducer for processing. Fetal heart structures moving toward the transducer reflect ultrasound waves at a higher frequency than the outgoing signal, whereas structures moving away from the transducer reflect ultrasound waves at a lower frequency. These changes in frequency, known as Doppler shift or Doppler effect, produce phasic signals that are converted into a graphic display of the FHR in a process similar to that used in direct monitoring ( Fig. 15-2 ). The raw signals produced by an external ultrasound transducer are more prone to artifact than those produced by a direct fetal ECG electrode. However, with improved computer processing and application of the autocorrelation technique, FHR tracings produced by modern external monitors are comparable to those produced by a direct fetal ECG electrode.

Instrumentation for external monitoring. Fetal heart rate (FHR) is monitored using the Doppler ultrasound transducer, which both emits and receives the reflected ultrasound signal that is then counted and recorded. Uterine contractions (UC) are detected by the pressure-sensitive tocodynamometer and are then amplified and recorded.

Indirect assessment of uterine activity is performed with a pressure transducer (tocodynamometer) applied tightly to the maternal abdomen over the uterine fundus. Uterine contractions change the shape and rigidity of the uterus and anterior abdominal wall, which generates pressure changes that are transmitted to the sensor located in the tocodynamometer transducer. Changes in pressure are converted into electrical signals and are plotted on the lower channel of the paper chart as a continuous display of uterine activity. When properly positioned on the maternal abdomen, the external tocodynamometer permits assessment of the relative frequency and duration of uterine contractions. However, it does not directly measure intrauterine pressure and therefore does not provide a reliable assessment of uterine contraction intensity or resting tone between contractions . When external uterine activity monitoring is used, contraction intensity and baseline uterine tone usually are assessed by palpation. Contraction strength is graded as mild, moderate, or strong depending upon the degree to which the uterine fundus can be indented by palpation with the fingertips during the peak of a uterine contraction. During mild contractions, the fundus is easily indented by the fingertips; during strong contractions, the fundus cannot be indented. If the fundus can be indented by intermediate pressure, the contraction strength is moderate.

External Environment

Oxygen comprises approximately 21% of inspired air. Therefore in inspired air, the partial pressure exerted by oxygen gas (PO ₂ ) is approximately 21% of total atmospheric pressure (760 mm Hg) minus the pressure exerted by water vapor (47 mm Hg). At sea level, this translates to approximately 150 mm Hg. As oxygen is transferred from the external atmosphere to maternal blood and then to fetal blood, the partial pressure progressively declines. By the time oxygen reaches fetal umbilical venous blood, the partial pressure may be as low as 30 mm Hg. After oxygen is delivered to fetal tissues, the PO ₂ of deoxygenated blood in the umbilical arteries returning to the placenta is approximately 15 to 25 mm Hg. The sequential transfer of oxygen from the environment to the fetus and potential causes of interruption at each step are described below.

Maternal Lungs

Inspiration carries oxygenated air from the external environment to the distal air spaces of the lungs, the alveoli. On the way to the alveoli, inspired air mixes with less oxygenated air leaving the lungs. As a result, the PO ₂ of air within the alveoli is lower than that in inspired air. At sea level, alveolar PO ₂ is approximately 100 to 105 mm Hg. From the alveoli, oxygen diffuses across a thin blood-gas barrier into the pulmonary capillary blood. This pulmonary blood-gas barrier consists of three layers: a single-cell layer of alveolar epithelium and basement membrane, a layer of extracellular matrix (interstitium), and a single-cell layer of pulmonary capillary endothelium and basement membrane. Interruption of oxygen transfer from the environment to the alveoli can result from airway obstruction or depression of central respiratory control caused by medications (narcotics, magnesium) or convulsions (apnea). Interruption of oxygen transfer from the alveoli to the pulmonary capillary blood can be caused by a number of factors that include ventilation-perfusion mismatch and diffusion defects due to conditions such as pulmonary embolus, pneumonia, asthma, atelectasis, or acute respiratory distress syndrome (ARDS).

Maternal Blood

After diffusing from the pulmonary alveoli into maternal blood, more than 98% of oxygen combines with hemoglobin in maternal red blood cells. The remaining 1% to 2% is dissolved in the blood and is measured by the partial pressure of oxygen in arterial blood (PaO ₂ ). The amount of oxygen bound to hemoglobin depends directly upon the PaO ₂ . Hemoglobin saturations at various PaO ₂ levels are illustrated by the oxyhemoglobin dissociation curve ( Fig. 15-4 ).

Maternal oxygen dissociation curve. The tendency for hemoglobin to release oxygen is increased by factors that signal an increased requirement for oxygen. Specifically, oxygen release is enhanced by factors that indicate active cellular metabolism. These factors shift the oxyhemoglobin saturation curve to the right and include anaerobic metabolism (reflected by increased 2,3-diphosphoglycerate concentration), production of lactic acid (reflected by decreased pH), aerobic metabolism (reflected by increased partial pressure of carbon dioxide [PCO ₂ ]), and heat.

A normal adult PaO ₂ value of 95 to 100 mm Hg results in a hemoglobin saturation of approximately 95% to 100%, indicating that hemoglobin is carrying 95% to 100% of the total amount of oxygen it is capable of carrying. A number of factors affect the affinity of hemoglobin for oxygen and can shift the oxyhemoglobin dissociation curve to the left or right. In general, the tendency for hemoglobin to release oxygen is increased by factors that signal an increased requirement for oxygen. Specifically, oxygen release is enhanced by factors that indicate active cellular metabolism. These factors shift the oxyhemoglobin saturation curve to the right and include by-products of anaerobic metabolism (reflected by increased 2,3-diphosphoglycerate [DPG] concentration), production of lactic acid (reflected by decreased pH), by-products of aerobic metabolism (reflected by increased partial pressure of carbon dioxide [PCO ₂ ]), and heat. Interruption of oxygen transfer from the environment to the fetus due to abnormal maternal oxygen-carrying capacity can result from severe anemia or from hereditary or acquired abnormalities that affect oxygen binding, such as hemoglobinopathies or methemoglobinemia. In an obstetric population, reduced maternal oxygen-carrying capacity is an uncommon cause of interrupted fetal oxygenation.

Maternal Heart

From the lungs, pulmonary veins carry oxygenated maternal blood to the heart. Pulmonary venous blood enters the left atrium with a PaO ₂ of approximately 95 to 100 mm Hg. Oxygenated blood passes from the left atrium through the mitral valve into the left ventricle and out the aorta for systemic distribution. Normal transfer of oxygen from the environment to the fetus is dependent upon normal cardiac function, reflected by cardiac output—the product of heart rate and stroke volume. Heart rate is determined by intrinsic cardiac pacemakers (sinoatrial node, atrioventricular node), the cardiac conduction system, autonomic regulation (sympathetic, parasympathetic), intrinsic humoral factors (catecholamines), extrinsic factors (medications), and local factors (calcium, potassium). Stroke volume is determined by preload, contractility, and afterload. Preload is the amount of stretch on myocardial fibers at the end of diastole when the ventricles are full of blood, and it is dependent on the volume of venous blood returning to the heart. Contractility is the force and speed with which myocardial fibers shorten during systole to expel blood from the heart. Afterload is the pressure that opposes the shortening of myocardial fibers during systole and is estimated by the systemic vascular resistance or systemic blood pressure.

Interruption of oxygen transfer from the environment to the fetus at the level of the maternal heart can be caused by any condition that reduces cardiac output, including altered heart rate (arrhythmia), reduced preload (hypovolemia, compression of the inferior vena cava), impaired contractility (ischemic heart disease, diabetes, cardiomyopathy, congestive heart failure), or increased afterload (hypertension). In addition, structural abnormalities of the heart and great vessels (valvular stenosis, valvular insufficiency, pulmonary hypertension, coarctation of the aorta) may impede its ability to pump blood. In a healthy obstetric patient, the most common cause of reduced cardiac output is reduced preload resulting from hypovolemia or compression of the inferior vena cava by the gravid uterus.

Maternal Vasculature

Oxygenated blood leaving the heart is carried by the systemic vasculature to the uterus. The vascular path includes the aorta, common iliac artery, internal iliac (hypogastric) artery, anterior division of the internal iliac artery, and the uterine artery. From the uterine artery, oxygenated blood travels through the arcuate, radial, and finally the spiral arteries before exiting the maternal vasculature and entering the intervillous space of the placenta. Interruption of oxygen transfer from the environment to the fetus at the level of the maternal vasculature commonly results from hypotension caused by regional anesthesia, hypovolemia, impaired venous return, impaired cardiac output, or medication . Alternatively, it may result from vasoconstriction of distal arterioles in response to endogenous vasoconstrictors or medications. Conditions associated with chronic vasculopathy—such as chronic hypertension, long-standing diabetes, collagen vascular disease, thyroid disease, or renal disease—may result in chronic suboptimal transfer of oxygen and nutrients to the fetus at the level of the maternal vasculature. Preeclampsia is associated with abnormal vascular remodeling at the level of the spiral arteries and can impede perfusion of the intervillous space. Acute vascular injuries (trauma, aortic dissection) are rare. In a healthy obstetric patient, transient hypotension is the most common cause of interrupted oxygen transfer at the level of the maternal vasculature. Chronic vascular conditions can exacerbate this interruption and should be considered in the course of thorough evaluation.

Uterus

Between the maternal uterine arteries and the intervillous space of the placenta, the arcuate, radial, and spiral arteries and their corresponding veins traverse the muscular wall of the uterus. Interruption of oxygen transfer from the environment to the fetus at the level of the uterus commonly results from uterine contractions that compress intramural blood vessels and impede the flow of blood. Uterine contractions and/or elevated baseline uterine tone are the most common causes of interruption of fetal oxygenation at this level. Uterine rupture is less common but must be considered in the appropriate clinical context.

Placenta

The placenta facilitates the exchange of gases, nutrients, wastes, and other molecules—for example antibodies, hormones, and medications—between maternal blood in the intervillous space and fetal blood in the villous capillaries. On the maternal side of the placenta, oxygenated blood exits the spiral arteries and enters the intervillous space to surround and bathe the chorionic villi. On the fetal side of the placenta, paired umbilical arteries carry blood from the fetus through the umbilical cord to the placenta. At term, the umbilical arteries receive 40% of fetal cardiac output . Upon reaching the placental cord insertion site, the umbilical arteries divide into multiple branches that fan out across the surface of the placenta. As illustrated in Figure 15-5 , at each cotyledon, placental arteries dive beneath the surface en route to the chorionic villi.

Placental blood flow.

The chorionic villi are microscopic branches of trophoblast that protrude into the intervillous space. Each villus is perfused by a fetal capillary bed that represents the terminal distribution of an umbilical artery. At term, fetal villous capillary blood is separated from maternal blood in the intervillous space by a thin blood-blood barrier similar to the blood-gas barrier in the maternal lung. The placental blood-blood barrier is comprised of a layer of placental trophoblast and a layer of fetal capillary endothelium with intervening basement membranes separated by a layer of villous stroma. Substances are exchanged between maternal and fetal blood by a number of mechanisms, including simple diffusion, facilitated diffusion, active transport, bulk flow, pinocytosis, and leakage. Examples of these mechanisms are summarized in Table 15-1 . Oxygen is transferred from the intervillous space to the fetal blood by a process that depends upon the PaO ₂ of maternal blood perfusing the intervillous space, the flow of oxygenated maternal blood into and out of the intervillous space, the chorionic villous surface area, and the rate of oxygen diffusion across the placental blood-blood barrier.

Intervillous Space PaO ₂

Oxygenated maternal blood leaves the maternal heart with a partial pressure of oxygen dissolved in arterial blood (PaO ₂ ) of approximately 95 to 100 mm Hg. Exiting the spiral arteries to perfuse the intervillous space of the placenta, oxygenated maternal blood has a PaO ₂ of approximately 95 to 100 mm Hg. Oxygen is released from maternal hemoglobin and diffuses across the placental blood-blood barrier into fetal blood, where it combines with fetal hemoglobin. As a result, maternal blood in the intervillous space becomes relatively oxygen depleted and exits the intervillous space via uterine veins with a PaO ₂ of approximately 40 mm Hg ( Fig. 15-6 ).

Uterine and umbilical blood gas values.

(From Miller LA, Miller DA, Martin Tucker S. Mosby’s Pocket Guide to Fetal Monitoring: A Multidisciplinary Approach. St. Louis: Elsevier; 2012.)

The average PaO ₂ of maternal blood in the intervillous space is between the PaO ₂ of blood entering the intervillous space (95 to 100 mm Hg) and the PaO ₂ of blood exiting the intervillous space (40 mm Hg). The average intervillous space PaO ₂ is in the range of 45 mm Hg . Interruption of fetal oxygenation can result from conditions that reduce the PaO ₂ of maternal blood entering the intervillous space. These conditions have been discussed previously.

Fetal Blood

After oxygen has diffused from the intervillous space across the placental blood-blood barrier and into fetal blood, the venous PO ₂ is in the range of 30 mm Hg, and fetal hemoglobin saturation is between 50% and 70%. Although fetal PO ₂ and hemoglobin saturation values are low in comparison to adult values, adequate delivery of oxygen to the fetal tissues is maintained by a number of compensatory mechanisms. For example, fetal cardiac output per unit weight is greater than that of the adult. Hemoglobin concentration and affinity for oxygen are greater in the fetus as well, resulting in increased oxygen-carrying capacity. Finally, oxygenated blood is directed preferentially toward vital organs by way of laminar blood flow and anatomic shunts at the level of the ductus venosus and foramen ovale. Conditions that can interrupt the transfer of oxygen from the environment to the fetus at the level of the fetal blood are uncommon but may include fetal anemia and reduced oxygen-carrying capacity secondary to alloimmunization, hemoglobinopathy, glucose-6-phosphate dehydrogenase (G6PD) deficiency, viral infections, fetomaternal hemorrhage, methemoglobinemia, or bleeding vasa previa.

Umbilical Cord

After oxygen binds to fetal hemoglobin in the villous capillaries, oxygenated blood returns to the fetus by way of villous veins that coalesce to form placental veins on the surface of the placenta. Placental surface veins unite to form a single umbilical vein within the umbilical cord . Interruption of the transfer of oxygen from the environment to the fetus at the level of the umbilical cord can result from simple mechanical compression. Other uncommon causes may include vasospasm, thrombosis, atherosis, hypertrophy, hemorrhage, inflammation, or a true “knot.” From the environment to the fetus, maternal and fetal blood carries oxygen along the oxygen pathway illustrated in Figure 15-3 . Examples of causes of interrupted oxygen transfer at each step along the pathway are summarized in Table 15-2 .

Gas exchange also involves the transfer of carbon dioxide in the opposite direction, from the fetus to the environment. Any condition that interrupts the transfer of oxygen from the environment to the fetus has the potential to interrupt the transfer of carbon dioxide from the fetus to the environment. However, carbon dioxide diffuses across the placental blood-blood barrier more rapidly than does oxygen; therefore any interruption of the pathway is likely to impact oxygen transfer to a greater extent than it does carbon dioxide transfer.

Mechanisms of Injury

If interruption of fetal oxygenation progresses to the stage of metabolic acidemia and hypotension, as described above, multiple organs and systems—including the brain and heart—can suffer hypoperfusion, reduced oxygenation, lowered pH, and reduced delivery of fuel for metabolism. These changes can contribute to a cascade of cellular events that include altered enzyme function, protease activation, ion shifts, altered water regulation, abnormal neurotransmitter metabolism, free radical production, and phospholipid degradation. Disruption of normal cellular metabolism can to lead to cellular and tissue dysfunction, injury, and even death.

Injury Threshold

The relationship between fetal oxygen deprivation and neurologic injury is complex. Electronic FHR monitoring was introduced with the hope that it would reduce the incidence of neurologic injury in the form of cerebral palsy (CP) caused by intrapartum interruption of fetal oxygenation. Subsequently, it has become apparent that most cases of CP are unrelated to intrapartum events and therefore cannot be prevented by modification of intrapartum management, including FHR monitoring. Nevertheless, some cases of CP may be linked to events during labor and delivery; therefore it is important to understand, to the extent possible, the relationship between intrapartum fetal oxygenation and the subsequent development of CP. In 1999, the International Cerebral Palsy Task Force published a consensus statement identifying essential criteria to establish intrapartum interruption of fetal oxygenation as a possible cause of CP. In January of 2003, The American College of Obstetricians and Gynecologists (ACOG) and the American Academy of Pediatrics (AAP) Cerebral Palsy Task Force published a monograph entitled “Neonatal Encephalopathy and Cerebral Palsy: Defining the Pathogenesis and Pathophysiology,” which summarized the literature regarding the relationship between intrapartum events and neurologic injury. Agencies and professional organizations that endorsed the ACOG-AAP task force report include the Centers for Disease Control and Prevention (CDC), the Child Neurology Society, the March of Dimes Birth Defects Foundation, the National Institute of Child Health and Human Development (NICHD), the Royal Australian and New Zealand College of Obstetricians and Gynecologists, the Society for Maternal-Fetal Medicine (SMFM), and the Society of Obstetricians and Gynaecologists of Canada.

The consensus report established four essential criteria to define an acute intrapartum hypoxic event sufficient to cause CP ( Box 15-1 ). The first criterion identified significant umbilical artery metabolic acidemia at birth (pH <7.0 and base deficit ≥12 mmol/L) as an essential prerequisite to establish a possible link between intrapartum interruption of fetal oxygenation and the later diagnosis of CP. It is important to recognize that even when significant metabolic acidemia is present, neonatal encephalopathy and fetal neurologic injury are uncommon. Respiratory acidemia without a metabolic component is not a significant risk factor for fetal neurologic injury.

The second criterion emphasized that in the absence of moderate to severe neonatal encephalopathy, intrapartum interruption of fetal oxygenation is very unlikely to result in CP. Neonatal encephalopathy has many possible causes. Hypoxic-ischemic encephalopathy (HIE) resulting from intrapartum interruption of fetal oxygenation represents only a small subset of neonatal encephalopathy, and most cases of HIE do not result in permanent neurologic injury.

The third criterion acknowledged that different subtypes of CP have different potential origins. The spastic quadriplegic subtype of CP caused by injury to the parasagittal cortex is characterized by abnormal motor control of all four extremities. The dyskinetic subtype of CP associated with injury to the basal ganglia involves disorganized, choreoathetoid movements. Although the presence of these CP subtypes does not constitute conclusive evidence of intrapartum hypoxic injury, they are the only subtypes that have been linked to hypoxic-ischemic neurologic injury at term. Other CP subtypes such as spastic diplegia, hemiplegia, ataxia, and hemiparetic CP are unlikely to result from acute intrapartum hypoxia. Conditions such as epilepsy, mental retardation, and attention-deficit/hyperactivity disorder do not result from intrapartum fetal hypoxia in the absence of CP.

The fourth criterion highlighted the fact that hypoxic-ischemic injury due to intrapartum interruption of fetal oxygenation is a potential cause of a relatively small subset of all cases of CP. Other identifiable etiologies include trauma, coagulation disorders, vascular accidents, infectious conditions, and genetic disorders. The 2003 ACOG-AAP Cerebral Palsy Task Force report further identified five criteria to help establish the timing of injury, emphasizing that these criteria are not specific to hypoxic-ischemic injury. These criteria are summarized in Box 15-2 .

In 2014, the ACOG-AAP Neonatal Encephalopathy Task Force revisited the scientific evidence linking intrapartum events, neonatal encephalopathy and subsequent neurologic outcome. The resulting monograph, Neonatal Encephalopathy and Neurologic Outcome (Second Edition), reaffirmed the concept that the pathway from intrapartum hypoxic-ischemic injury to subsequent CP must progress through neonatal encephalopathy. The report also reaffirmed the conclusion that spastic quadriplegia and dyskinetic CP are the subtypes most likely to be associated with hypoxic intrapartum injury at term. These conditions were not identified as absolute requirements for the diagnosis of intrapartum hypoxic neurologic injury. The 2014 report further concluded that “unless the newborn has accumulated significant metabolic acidemia, the likelihood of subsequent neurologic and cardiovascular morbidities attributable to perinatal events is low,” and “in a fetus exhibiting either moderate variability or accelerations of the FHR, damaging degrees of hypoxia-induced metabolic acidemia can reliably be excluded.” Unlike its predecessor, the 2014 task force report did not identify metabolic acidemia as an absolute requirement to diagnose intrapartum hypoxic neurologic injury.

Definitions and General Considerations

The standardized definitions proposed by the NICHD in 1997 and reiterated in 2008 apply to the interpretation of FHR patterns, produced either by a direct fetal electrode that detects the fetal ECG or by an external Doppler device that detects fetal cardiac motion using the autocorrelation technique, a computerized method of minimizing the artifact associated with Doppler ultrasound calculation of the FHR, a feature incorporated in all modern FHR monitors. Other important general considerations are as follows:

• •
  

  Patterns are categorized as baseline, periodic, or episodic.

  
  
• •
  

  Baseline patterns include baseline rate and variability.

  
  
• •
  

  Periodic and episodic patterns include FHR accelerations and decelerations.

  
  
• •
  

  Periodic patterns are those associated with uterine contractions.

  
  
• •
  

  Episodic patterns are those not associated with uterine contractions.

  
  
• •
  

  Deceleration onset is defined as abrupt if the onset to nadir (lowest point) is less than 30 seconds and gradual if the onset to nadir is 30 seconds or greater.

  
  
• •
  

  Although terms such as beat-to-beat variability, short-term variability, and long-term variability are used frequently in clinical practice, the NICHD panel recommended that no distinction be made between short-term or beat-to-beat variability and long-term variability because in actual practice, they are visually determined as a unit.

  
  
• •
  

  A number of FHR characteristics are dependent upon gestational age, so gestational age must be considered in the full evaluation of the pattern.

  
  
• •
  

  In addition, the FHR tracing should be evaluated in the context of maternal medical condition, prior results of fetal assessment, medications, and other factors.

  
  
• •
  

  FHR patterns do not occur alone and generally evolve over time. Therefore a full description requires a qualitative and quantitative assessment of baseline rate, variability, accelerations, decelerations, sinusoidal pattern, and changes or trends over time.

Specific Fetal Heart Rate Patterns

Understanding the common FHR patterns and characteristics is fundamental to the interpretation of these as they relate to intrapartum care. As decribed above, intrapartum FHR monitoring is critical to ensuring fetal and maternal well-being.

Baseline Rate

Definition

Baseline FHR is defined as the approximate mean FHR rounded to increments of 5 beats/min during a 10-minutes segment excluding accelerations, decelerations, and periods of marked variability. In any 10-minute window, the minimum baseline duration must be at least 2 minutes—not necessarily contiguous—or the baseline for that period is deemed inde­terminate. If the baseline during any 10-minute segment is deemed indeterminate, it may be necessary to refer to any pre­vious 10-minute segments for determination of the baseline ( Fig. 15-7 ).

Baseline fetal heart rate (FHR) is the mean FHR rounded to increments of 5 beats/min in a 10-minute window excluding accelerations, decelerations, and periods of marked FHR variability (>25 beats/min). At least 2 minutes of identifiable baseline segments, not necessarily contiguous, must be present in any 10-minute window or the baseline for that period is indeterminate. In this tracing, the baseline heart rate is 120 beats/min with accelerations.

Physiology

Baseline FHR is regulated by intrinsic cardiac pacemakers (sinoatrial node, atrioventricular node), cardiac conduction pathways, autonomic innervation (sympathetic, parasympathetic), intrinsic humoral factors (catecholamines), extrinsic factors (medications), and local factors (calcium, potassium). Sympathetic innervation and plasma catecholamines increase baseline FHR, whereas parasympathetic innervation reduces the baseline rate. Autonomic input regulates the FHR in response to fluctuations in the partial pressure of oxygen (PO ₂ ), partial pressure of carbon dioxide (PCO ₂ ), and blood pressure detected by chemoreceptors and baroreceptors located in the aortic arch and carotid arteries. A normal FHR baseline of 110 to 160 beats/min is consistent with normal neurologic regulation of the FHR. Fetal tachycardia is defined as a baseline rate above 160 beats/min for at least 10 minutes . Conditions potentially associated with fetal tachycardia are summarized in Box 15-5 .

Box 15-5

Conditions Potentially Associated with Fetal Tachycardia

• 
  

  Maternal fever

  
  
• 
  

  Infection

  
  
• 
  

  Medications/drugs

  
  
  
  
  • •
    

    Sympathomimetics

    
    
  • •
    

    Parasympatholytics

    
    
  • •
    

    Caffeine

    
    
  • •
    

    Theophylline

    
    
  • •
    

    Cocaine

    
    
  • •
    

    Methamphetamine

  
  
  
  
• 
  

  Fetal anemia

  
  
• 
  

  Hyperthyroidism

  
  
• 
  

  Arrhythmia

  
  
  
  
  • •
    

    Sinus tachycardia

    
    
  • •
    

    Supraventricular tachycardia

    
    
  • •
    

    Atrial fibrillation

    
    
  • •
    

    Atrial flutter

    
    
  • •
    

    Ventricular arrhythmia

  
  
  
  
• 
  

  Metabolic acidemia

Fetal bradycardia is defined as a baseline rate below 110 beats/min for at least 10 minutes. Box 15-6 summarizes conditions associated with fetal bradycardia.

Box 15-6

Conditions Potentially Associated with Fetal Bradycardia

• 
  

  Medications

  
  
  
  
  • •
    

    Sympatholytics

    
    
  • •
    

    Parasympathomimetics

  
  
  
  
• 
  

  Cardiac pacing and conduction abnormalities

  
  
  
  
  • •
    

    Heart block

    
    
  • •
    

    Sjögren antibodies

    
    
  • •
    

    Heterotaxy syndrome

  
  
  
  
• 
  

  Structural cardiac defects

  
  
• 
  

  Viral infections (e.g., cytomegalovirus)

  
  
• 
  

  Fetal heart failure

  
  
• 
  

  Maternal hypoglycemia

  
  
• 
  

  Maternal hypothermia

  
  
• 
  

  Interruption of fetal oxygenation

Variability

Definition

Variability is defined as fluctuations in the baseline FHR that are irregular in amplitude and frequency. Variability is measured from the peak to the trough of the fluctuations and is quantitated in beats per minute. No distinction is made between short-term (beat-to-beat) variability and long-term variability because in actual practice, they are visually determined as a unit. In addition, there is no consensus that beat-to-beat differences in rate can be quantitated accurately with the unaided eye. Standardized NICHD nomenclature classifies variability as absent, minimal, moderate, or marked. As depicted in Figure 15-8 , variability is defined as absent when the amplitude range of the FHR fluctuations is undetectable to the unaided eye. Variability is defined as minimal when the amplitude range is visually detectable but is less than or equal to 5 beats/min, as illustrated in Figure 15-9 . When the amplitude range of the FHR fluctuations is 6 to 25 beats/min, variability is defined as moderate, as illustrated in Figure 15-10 . Variability is defined as marked when the amplitude range of the FHR fluctuations is greater than 25 beats/min ( Fig. 15-11 ).

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