Seminars in Fetal & Neonatal Medicine xxx (2015) 1e5
Contents lists available at ScienceDirect
Seminars in Fetal & Neonatal Medicine journal homepage: www.elsevier.com/locate/siny
Fetal heart rate monitoring Michael P. Nageotte* Miller Children's and Women's Hospital, Long Beach, 2801 Atlantic Avenue, Long Beach, CA 90801, USA
s u m m a r y Keywords: Electronic fetal monitoring Category I, II and III fetal tracings Late decelerations Variable decelerations Sinusoidal
Electronic fetal heart rate monitoring is a widely utilized means of assessment of fetal status during labor. Whereas little evidence exists regarding efficacy, this modality continues to be used extensively in every modern labor and delivery unit in developed countries. It is of importance that all providers of health care to the woman in labor and her newborn have a clear understanding of the basic pathophysiology of fetal heart rate monitoring and an appreciation for labor course and concerns as they arise in order to optimize outcomes and patient safety. © 2015 Elsevier Ltd. All rights reserved.
1. Introduction Electronic fetal heart rate monitoring (EFM) is widely used in nearly every modern labor and delivery unit in the developed world, and was initially introduced for clinical use in the late 1960s as an alternative to the very labor-intensive auscultation of the fetal heart. EFM uses either the direct electrical signal of the fetal heart rate captured through a fetal electrode (direct) or more usually employs ultrasound technology and Doppler physics to interpret the changes in frequency of sound waves reflected from pulsations within fetal vessels (indirect). The aim of such monitoring, which is generally continuous, is to enable clinicians to accurately identify hypoxic fetuses at risk for deterioration and who might benefit from expedited or immediate delivery either vaginally or by Cesarean section. Whereas EFM remains an accepted component of labor management and fetal assessment, the true positive predictive value for metabolic acidosis is low. Unfortunately, this often results in unnecessary interventions and a significant increase in the Cesarean section rate for concerns regarding fetal intolerance of labor. Such an observation may be the result of appropriate early intervention before worsening of metabolic condition occurs or inappropriate early intervention from a misreading of the information generated from the fetal monitor. Whereas the negative predictive value is exceptionally high (a normal fetal heart rate is associated with a normally oxygenated and non-acidotic fetus) and the rate of unexpected intrapartum stillbirth approaches zero, nonetheless, despite the wide usage of EFM, unfortunately there
* Tel.: þ1 562 933 2738; fax: þ1 562 933 2740. E-mail address: [email protected].
has been no significant decrease in the incidence of long-term neurologic morbidity (including cerebral palsy) or several other measures of neonatal wellbeing for the term newborn [1]. Despite these factors, EFM will continue to be utilized and needs to be understood with clinical concerns clearly communicated to provide the best care to all patients during pregnancy and in labor. Every member of the health care team needs to have an understanding of the suspected fetal status, which is often directly related to findings of changes in the fetal heart monitor so care can be best coordinated and effectively rendered in both non-emergency and emergency situations. 2. Physiologic basis of fetal monitoring Fetal heart rate monitoring is essentially an observation of ongoing human fetal physiology, most often during labor or prior to labor, in the assessment of patients with certain high-risk conditions for which antepartum fetal surveillance is indicated. The question asked in all situations is: what is the adequacy of fetal oxygenation at this point? Since there are certain characteristic changes in the fetal heart rate pattern resulting from various hypoxic and non-hypoxic influences, one needs to appreciate the basic physiology of fetal respiratory exchange and resultant control of the fetal heart rate. The placenta functions as an extracorporeal support system for the human fetus, serving as the fetal lung (respiratory exchange), kidney (excretion), gastrointestinal tract (nutrition) and skin surface (heat exchange). In addition, it plays a critical role in protecting the fetus against certain substances in the maternal circulation, which may be harmful particularly during early gestation. Further, the placenta actively produces several steroid and protein
http://dx.doi.org/10.1016/j.siny.2015.02.002 1744-165X/© 2015 Elsevier Ltd. All rights reserved.
Please cite this article in press as: Nageotte MP, Fetal heart rate monitoring, Seminars in Fetal & Neonatal Medicine (2015), http://dx.doi.org/ 10.1016/j.siny.2015.02.002
2
M.P. Nageotte / Seminars in Fetal & Neonatal Medicine xxx (2015) 1e5
hormones critical to successful maintenance of the gestation and initiation of parturition. The human placenta is termed a hemochorial type, since maternal blood is extravascular when it comes into contact with the fetal chorionic villus. Exchange of oxygen, carbon dioxide, nutrients, water, heat, and waste products occurs within the placenta and must cross two layers of fetal trophoblast, the fetal connective tissue within the villus and the fetal capillary wall. Maternal blood flow to the uterus, and in turn to the placenta, results principally from the uterine arteries as well as from the internal iliac and ovarian arteries, and it markedly increases over the course of pregnancy. The arteries feeding the intervillous space where fetalematernal exchange occurs are termed spiral arteries, and they must traverse the maternal myometrium. Flow through these spiral arteries is directly affected by anything that influences maternal cardiac output (e.g., hypotension, hemorrhage, sepsis) with immediate changes noted in the fetal heart rate in response to the decrease in uterine blood flow. Further and most importantly, as the uterus contracts, the pressure generated within the myometrium may exceed the intra-arterial pressure of the spiral arteries, resulting in intermittent cessation of maternal blood flow into the intervillous space. If such stasis is prolonged or associated with a significantly compromised placenta (small, infarcted, inflamed or senescent), either acute or chronic episodes of hypoxia and potentially acidosis in the fetus may result. Such changes are reflected in specific pattern changes in the fetal heart rate. Further, these conditions may be mitigated by position change of the mother to a lateral position or by directly addressing and correcting the causes of the compromised maternal cardiac output. The fetus also responds to such challenges by redistributing blood flow to certain vital organs e such as the brain, the heart, and the adrenal glands e while diminishing blood flow to less vital organs including the lungs, liver, kidneys, intestine, and periphery. However, if such changes persist, there may be a loss of cerebral autoregulation as well as an eventual decrease in fetal cardiac output. Cerebral blood flow is maintained initially by a fall in fetal cerebral vascular resistance by as much as 50%. However, if the physiologic condition continues to be compromised or worsens, then a reduction of cerebral blood flow may result, leading to potential fetal neuronal injury or death. 3. Essentials of fetal heart rate regulation Just as in the adult, the fetal heart rate results from the influences of various intrinsic and extrinsic factors that modify the rate. The heart rate is actually the reciprocal of the interval between successive heart contractions. EFM uses the peak of the fetal electrocardiogram (ECG) R-wave to signify the time of the beat. The rate is then calculated by the interval between consecutive fetal ECG Rwaves when using direct fetal electrodes, while it is calculated between consecutive pulse waves generated by myocardial contractions when using external monitoring employing ultrasound technology. It is the change in the fetal heart rate that is observed in various conditions that constitutes the basis of EFM, and one must appreciate the various factors that influence or modify the fetal heart rate to be able to correctly interpret the patterns generated by the fetal monitor. The baseline heart rate of the fetus must be established to correctly interpret fetal tracings. Baseline heart rate decreases with advancing gestational age, being higher in early pregnancy than later. Further, the normal rate for the baseline is between 110 and 160 beats per minute (bpm). Such a rate results normally from the atrial pacemaker with modulation by parasympathetic and sympathetic factors. Rarely seen are cases of complete fetal heart block (with the rate usually about 60 bpm) resulting from the intrinsic ventricular or nodal rate.
In addition to baseline heart rate, key to interpreting EFM is the variability of the baseline heart rate. Variability is the true variance in time between consecutive heart beats, and it is normally present in a healthy fetus. Variability results from direct sympathetic and parasympathetic effects on the heart, which originate either in the brain stem and are conducted to the heart via the vagus nerve, or may arise from direct humoral stimulation of cardiac receptors responding to the release of epinephrine from the fetal adrenal glands. It is thought that higher brain centers also play a role in variability of the heart rate. Factors that influence the central nervous system such as drugs, hypoxia, metabolic acidosis, or brain injury affect the baseline variability of the heart rate. The presence of moderate variability of the heart rate is one of the most reliable markers of normal oxygenation and absence of acidosis, and its presence or absence is key to the correct interpretation of EFM. A normally oxygenated fetus has certain characteristics of its heart rate. After 32 weeks of gestation, it is well established that normal fetuses have episodes of acceleration of their heart rate associated with fetal movements. This is termed “reactivity”, and, when present, has a very high association with a normal fetal state of oxygenation. Whereas there is not necessarily an acceleration of the heart rate every time a fetus moves, the converse is true. A normally oxygenated fetus generally demonstrates accelerations at least every 60e80 min. Certain drugs that affect the central nervous system can suppress accelerations, as can certain types of primary central nervous system abnormalities. A basic tenet that has been demonstrated experimentally is that in a fetus undergoing progressive hypoxia, there will be the appearance of decelerations before the absence of accelerations. Fetal monitoring is assessed both in the absence and in the presence of uterine contractions. As discussed, a uterine contraction may cause intermittent decreases in maternal blood flow into the intervillous space. This may result in stasis of blood with inadequate exchange between the mother and fetus of oxygen, carbon dioxide, and other products. If significant hypoxia of the fetus occurs, there may be a decrease in fetal cerebral blood flow, resulting in a change of the sympathetic and parasympathetic control of the fetal heart. This may lead to a slowing of the fetal heart rate or a deceleration. Another frequently occurring mechanism explaining the occurrence of the deceleration is intermittent occlusion of blood flow through the umbilical cord due to cord compression or stretching. Such changes, particularly when associated with uterine activity, are considered contraction-related or “periodic” changes in the fetal heart rate. Again, key to interpretation of these changes in the fetal heart rate is the understanding of their physiologic bases.
4. Early decelerations An early deceleration is a uniformly shaped deceleration of gradual onset and gradual return to baseline associated with a uterine contraction. The degree of slowing generally is proportional to the strength of the associated uterine contraction, and the timing of the deceleration accompanying the uterine contraction generally mirrors the contraction with the early deceleration nadir at the peak of the contraction. Early decelerations are thought to result from fetal head compression altering cerebral blood flow and leading to cardiac slowing through a vagal reflex. This is supported by the experimental finding that early decelerations can be abolished or altered by the administration of atropine. Early decelerations are generally seen in active labor and are a pattern not associated with fetal hypoxia, acidosis, or subsequent depressed Apgar scores.
Please cite this article in press as: Nageotte MP, Fetal heart rate monitoring, Seminars in Fetal & Neonatal Medicine (2015), http://dx.doi.org/ 10.1016/j.siny.2015.02.002
M.P. Nageotte / Seminars in Fetal & Neonatal Medicine xxx (2015) 1e5
5. Variable decelerations The most common deceleration of the fetal heart rate is the variable deceleration. Variable decelerations frequently occur in both the first and second stages of labor and are usually indicative of some degree of obstruction to fetal blood flow through the umbilical cord or compression of the vessels within the cord. Again, the mechanism of such deceleration is thought to be mediated through the vagus nerve and often bears no temporal relationship to uterine contractions. Hypoxia is clearly not required to produce variable decelerations, as changes in fetal blood pressure associated with umbilical cord compression alone can produce such patterns. Data from studies using continuous fetal pulse oximetry also have demonstrated that deep and relatively prolonged variable decelerations occur often without any change in fetal oxygen saturation. Pregnancies complicated with decreased amniotic fluid (oligohydramnios) are associated with more frequent patterns of variable decelerations, and this is thought to be related to the loss of the protective effect of the amniotic fluid on the fetal umbilical cord. Such a relationship is further supported by the fact that, in cases with diminished amniotic fluid in labor treated with saline amnio-infusion via a transcervical catheter, there is a reduction in the frequency of variable decelerations in both preterm and term fetuses compared to controls [2]. Variable decelerations characteristically are very abrupt in onset and return to baseline. They may be associated with fetal movement or uterine contractions and are most commonly seen in the second stage of labor associated with maternal Valsalva and pushing efforts. Variable decelerations have different degrees of decrease of heart rate, time below baseline, and rate of return to baseline. The vast majority of variable decelerations are not associated with significant hypoxia or acidosis. Because of their frequency and unpredictability, variable decelerations must be evaluated and managed closely. With cord compression that is prolonged and repetitive, there may be the development of progressive fetal hypoxia and respiratory acidosis. Thus, variable decelerations have been graded as mild, moderate, and severe. Mild variable decelerations last for 2 min. Such a decrease must be 15 bpm below baseline and last 80% of fetuses in labor demonstrate at times Category II patterns [7]. Recently, specific management proposals for Category II tracings have been recommended and generally utilized [8]. These include the use of various algorithms for management depending upon the presence or absence of variability or accelerations of the fetal heart rate, the presence or absence of significant decelerations, the stage of labor, and evidence of normal progress in labor. 11. Conclusion The use of EFM continues to be ubiquitous in modern labor and delivery units. Whereas there is no clear consensus regarding strict guidelines for the clinical management of all patients using specific fetal heart rate patterns, there is little variation in opinion about the definition of distinctly normal and abnormal patterns. Most fetuses demonstrate patterns of heart rate during labor that are intermediate between these extremes. In such a setting, the specific clinical management and presumed fetal status are controversial and there is not one accepted standard of care for management. With such a background, it is imperative that clinical concerns regarding fetal or maternal status must be clearly documented and shared among all members of the health care team. This includes clear communication among the physicians and nurses managing the patient, as well as with the neonatal team tasked with caring for and at times emergently resuscitating the newborn. Whereas strides have been clearly made toward eliminating the cases of unexpected intrapartum stillbirth, the use of continuous EFM remains a challenge in the appropriate interpretation, application, and credentialing of those who utilize it in an effort to safeguard the mother and her fetus during the process of parturition.
Practice points EFM is a highly reliable assessment of normal fetal oxygenation when it is Category I. Over the course of labor, the fetal heart rate will often change between Categories I and II and does not necessarily suggest any significant worsening of fetal status. Category III fetal heart rate patterns are most concerning, correlate highly with need for neonatal resuscitation, and need to be acted upon with either improvement or delivery of the fetus.
Please cite this article in press as: Nageotte MP, Fetal heart rate monitoring, Seminars in Fetal & Neonatal Medicine (2015), http://dx.doi.org/ 10.1016/j.siny.2015.02.002
M.P. Nageotte / Seminars in Fetal & Neonatal Medicine xxx (2015) 1e5
5
References Research directions There needs to be ongoing research into new technologies that may serve as adjuncts to EFM for fetal assessment. Studies utilizing proposed management strategies for Category II tracing must be done to provide evidence that such strategies are appropriate. Use of a common language and intrapartum management approach must be stressed for each institution providing labor and delivery services, as well as monitoring to insure patient safety and improved perinatal outcomes.
Conflict of interest statement None declared. Funding sources
[1] Freeman RK. Intrapartum fetal monitoring e a disappointing story. N Engl J Med 1990;322:624e6. [2] Nageotte MP, Freeman RK, Garite TJ, Dorchester W. Prophylactic intrapartum amnioinfusion in patients with preterm premature rupture of membranes. Am J Obstet Gynecol 1985;153:557e62. [3] Hon EH. Observations on “pathologic” fetal bradycardia. Am J Obstet Gynecol 1959;77:1084e8. [4] Caldeyro-Bacia R, Casaciberta C, Bustos R, Giussi G, Gulin L, Escarcena L, et al. Correlation of intrapartum changes in fetal heart rate with fetal blood oxygen and acid base state. In: Adamsons K, editor. Diagnosis and treatment of fetal disorders. New York: Springer-Verlag; 1968. p. 205e25. [5] Murata Y, Miyake Y, Yamamoto T, Higuchi M, Hesser J, Ibara S, et al. Experimentally produced sinusoidal fetal heart rate pattern in the chronically instrumented fetal lamb. Am J Obstet Gynecol 1985;153:693e6. [6] Macones GA, Hankins GD, Spong CY, Hauth J, Moore T. 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;112:661e6. [7] American College of Obstetricians and Gynecologists. Management of intrapartum fetal heart rate tracings: ACOG practice bulletin no. 116. Obstet Gynecol 2010;116:1232e40. [8] Clark SL, Nageotte MP, Garite TJ, Freeman RK, Miller DA, Simpson KR, et al. Intrapartum management of category II fetal heart rate tracings: towards standardization of care. Am J Obstet Gynecol 2013;209:89e97.
None.
Please cite this article in press as: Nageotte MP, Fetal heart rate monitoring, Seminars in Fetal & Neonatal Medicine (2015), http://dx.doi.org/ 10.1016/j.siny.2015.02.002
Contents lists available at ScienceDirect
Seminars in Fetal & Neonatal Medicine journal homepage: www.elsevier.com/locate/siny
Fetal heart rate monitoring Michael P. Nageotte* Miller Children's and Women's Hospital, Long Beach, 2801 Atlantic Avenue, Long Beach, CA 90801, USA
s u m m a r y Keywords: Electronic fetal monitoring Category I, II and III fetal tracings Late decelerations Variable decelerations Sinusoidal
Electronic fetal heart rate monitoring is a widely utilized means of assessment of fetal status during labor. Whereas little evidence exists regarding efficacy, this modality continues to be used extensively in every modern labor and delivery unit in developed countries. It is of importance that all providers of health care to the woman in labor and her newborn have a clear understanding of the basic pathophysiology of fetal heart rate monitoring and an appreciation for labor course and concerns as they arise in order to optimize outcomes and patient safety. © 2015 Elsevier Ltd. All rights reserved.
1. Introduction Electronic fetal heart rate monitoring (EFM) is widely used in nearly every modern labor and delivery unit in the developed world, and was initially introduced for clinical use in the late 1960s as an alternative to the very labor-intensive auscultation of the fetal heart. EFM uses either the direct electrical signal of the fetal heart rate captured through a fetal electrode (direct) or more usually employs ultrasound technology and Doppler physics to interpret the changes in frequency of sound waves reflected from pulsations within fetal vessels (indirect). The aim of such monitoring, which is generally continuous, is to enable clinicians to accurately identify hypoxic fetuses at risk for deterioration and who might benefit from expedited or immediate delivery either vaginally or by Cesarean section. Whereas EFM remains an accepted component of labor management and fetal assessment, the true positive predictive value for metabolic acidosis is low. Unfortunately, this often results in unnecessary interventions and a significant increase in the Cesarean section rate for concerns regarding fetal intolerance of labor. Such an observation may be the result of appropriate early intervention before worsening of metabolic condition occurs or inappropriate early intervention from a misreading of the information generated from the fetal monitor. Whereas the negative predictive value is exceptionally high (a normal fetal heart rate is associated with a normally oxygenated and non-acidotic fetus) and the rate of unexpected intrapartum stillbirth approaches zero, nonetheless, despite the wide usage of EFM, unfortunately there
* Tel.: þ1 562 933 2738; fax: þ1 562 933 2740. E-mail address: [email protected].
has been no significant decrease in the incidence of long-term neurologic morbidity (including cerebral palsy) or several other measures of neonatal wellbeing for the term newborn [1]. Despite these factors, EFM will continue to be utilized and needs to be understood with clinical concerns clearly communicated to provide the best care to all patients during pregnancy and in labor. Every member of the health care team needs to have an understanding of the suspected fetal status, which is often directly related to findings of changes in the fetal heart monitor so care can be best coordinated and effectively rendered in both non-emergency and emergency situations. 2. Physiologic basis of fetal monitoring Fetal heart rate monitoring is essentially an observation of ongoing human fetal physiology, most often during labor or prior to labor, in the assessment of patients with certain high-risk conditions for which antepartum fetal surveillance is indicated. The question asked in all situations is: what is the adequacy of fetal oxygenation at this point? Since there are certain characteristic changes in the fetal heart rate pattern resulting from various hypoxic and non-hypoxic influences, one needs to appreciate the basic physiology of fetal respiratory exchange and resultant control of the fetal heart rate. The placenta functions as an extracorporeal support system for the human fetus, serving as the fetal lung (respiratory exchange), kidney (excretion), gastrointestinal tract (nutrition) and skin surface (heat exchange). In addition, it plays a critical role in protecting the fetus against certain substances in the maternal circulation, which may be harmful particularly during early gestation. Further, the placenta actively produces several steroid and protein
http://dx.doi.org/10.1016/j.siny.2015.02.002 1744-165X/© 2015 Elsevier Ltd. All rights reserved.
Please cite this article in press as: Nageotte MP, Fetal heart rate monitoring, Seminars in Fetal & Neonatal Medicine (2015), http://dx.doi.org/ 10.1016/j.siny.2015.02.002
2
M.P. Nageotte / Seminars in Fetal & Neonatal Medicine xxx (2015) 1e5
hormones critical to successful maintenance of the gestation and initiation of parturition. The human placenta is termed a hemochorial type, since maternal blood is extravascular when it comes into contact with the fetal chorionic villus. Exchange of oxygen, carbon dioxide, nutrients, water, heat, and waste products occurs within the placenta and must cross two layers of fetal trophoblast, the fetal connective tissue within the villus and the fetal capillary wall. Maternal blood flow to the uterus, and in turn to the placenta, results principally from the uterine arteries as well as from the internal iliac and ovarian arteries, and it markedly increases over the course of pregnancy. The arteries feeding the intervillous space where fetalematernal exchange occurs are termed spiral arteries, and they must traverse the maternal myometrium. Flow through these spiral arteries is directly affected by anything that influences maternal cardiac output (e.g., hypotension, hemorrhage, sepsis) with immediate changes noted in the fetal heart rate in response to the decrease in uterine blood flow. Further and most importantly, as the uterus contracts, the pressure generated within the myometrium may exceed the intra-arterial pressure of the spiral arteries, resulting in intermittent cessation of maternal blood flow into the intervillous space. If such stasis is prolonged or associated with a significantly compromised placenta (small, infarcted, inflamed or senescent), either acute or chronic episodes of hypoxia and potentially acidosis in the fetus may result. Such changes are reflected in specific pattern changes in the fetal heart rate. Further, these conditions may be mitigated by position change of the mother to a lateral position or by directly addressing and correcting the causes of the compromised maternal cardiac output. The fetus also responds to such challenges by redistributing blood flow to certain vital organs e such as the brain, the heart, and the adrenal glands e while diminishing blood flow to less vital organs including the lungs, liver, kidneys, intestine, and periphery. However, if such changes persist, there may be a loss of cerebral autoregulation as well as an eventual decrease in fetal cardiac output. Cerebral blood flow is maintained initially by a fall in fetal cerebral vascular resistance by as much as 50%. However, if the physiologic condition continues to be compromised or worsens, then a reduction of cerebral blood flow may result, leading to potential fetal neuronal injury or death. 3. Essentials of fetal heart rate regulation Just as in the adult, the fetal heart rate results from the influences of various intrinsic and extrinsic factors that modify the rate. The heart rate is actually the reciprocal of the interval between successive heart contractions. EFM uses the peak of the fetal electrocardiogram (ECG) R-wave to signify the time of the beat. The rate is then calculated by the interval between consecutive fetal ECG Rwaves when using direct fetal electrodes, while it is calculated between consecutive pulse waves generated by myocardial contractions when using external monitoring employing ultrasound technology. It is the change in the fetal heart rate that is observed in various conditions that constitutes the basis of EFM, and one must appreciate the various factors that influence or modify the fetal heart rate to be able to correctly interpret the patterns generated by the fetal monitor. The baseline heart rate of the fetus must be established to correctly interpret fetal tracings. Baseline heart rate decreases with advancing gestational age, being higher in early pregnancy than later. Further, the normal rate for the baseline is between 110 and 160 beats per minute (bpm). Such a rate results normally from the atrial pacemaker with modulation by parasympathetic and sympathetic factors. Rarely seen are cases of complete fetal heart block (with the rate usually about 60 bpm) resulting from the intrinsic ventricular or nodal rate.
In addition to baseline heart rate, key to interpreting EFM is the variability of the baseline heart rate. Variability is the true variance in time between consecutive heart beats, and it is normally present in a healthy fetus. Variability results from direct sympathetic and parasympathetic effects on the heart, which originate either in the brain stem and are conducted to the heart via the vagus nerve, or may arise from direct humoral stimulation of cardiac receptors responding to the release of epinephrine from the fetal adrenal glands. It is thought that higher brain centers also play a role in variability of the heart rate. Factors that influence the central nervous system such as drugs, hypoxia, metabolic acidosis, or brain injury affect the baseline variability of the heart rate. The presence of moderate variability of the heart rate is one of the most reliable markers of normal oxygenation and absence of acidosis, and its presence or absence is key to the correct interpretation of EFM. A normally oxygenated fetus has certain characteristics of its heart rate. After 32 weeks of gestation, it is well established that normal fetuses have episodes of acceleration of their heart rate associated with fetal movements. This is termed “reactivity”, and, when present, has a very high association with a normal fetal state of oxygenation. Whereas there is not necessarily an acceleration of the heart rate every time a fetus moves, the converse is true. A normally oxygenated fetus generally demonstrates accelerations at least every 60e80 min. Certain drugs that affect the central nervous system can suppress accelerations, as can certain types of primary central nervous system abnormalities. A basic tenet that has been demonstrated experimentally is that in a fetus undergoing progressive hypoxia, there will be the appearance of decelerations before the absence of accelerations. Fetal monitoring is assessed both in the absence and in the presence of uterine contractions. As discussed, a uterine contraction may cause intermittent decreases in maternal blood flow into the intervillous space. This may result in stasis of blood with inadequate exchange between the mother and fetus of oxygen, carbon dioxide, and other products. If significant hypoxia of the fetus occurs, there may be a decrease in fetal cerebral blood flow, resulting in a change of the sympathetic and parasympathetic control of the fetal heart. This may lead to a slowing of the fetal heart rate or a deceleration. Another frequently occurring mechanism explaining the occurrence of the deceleration is intermittent occlusion of blood flow through the umbilical cord due to cord compression or stretching. Such changes, particularly when associated with uterine activity, are considered contraction-related or “periodic” changes in the fetal heart rate. Again, key to interpretation of these changes in the fetal heart rate is the understanding of their physiologic bases.
4. Early decelerations An early deceleration is a uniformly shaped deceleration of gradual onset and gradual return to baseline associated with a uterine contraction. The degree of slowing generally is proportional to the strength of the associated uterine contraction, and the timing of the deceleration accompanying the uterine contraction generally mirrors the contraction with the early deceleration nadir at the peak of the contraction. Early decelerations are thought to result from fetal head compression altering cerebral blood flow and leading to cardiac slowing through a vagal reflex. This is supported by the experimental finding that early decelerations can be abolished or altered by the administration of atropine. Early decelerations are generally seen in active labor and are a pattern not associated with fetal hypoxia, acidosis, or subsequent depressed Apgar scores.
Please cite this article in press as: Nageotte MP, Fetal heart rate monitoring, Seminars in Fetal & Neonatal Medicine (2015), http://dx.doi.org/ 10.1016/j.siny.2015.02.002
M.P. Nageotte / Seminars in Fetal & Neonatal Medicine xxx (2015) 1e5
5. Variable decelerations The most common deceleration of the fetal heart rate is the variable deceleration. Variable decelerations frequently occur in both the first and second stages of labor and are usually indicative of some degree of obstruction to fetal blood flow through the umbilical cord or compression of the vessels within the cord. Again, the mechanism of such deceleration is thought to be mediated through the vagus nerve and often bears no temporal relationship to uterine contractions. Hypoxia is clearly not required to produce variable decelerations, as changes in fetal blood pressure associated with umbilical cord compression alone can produce such patterns. Data from studies using continuous fetal pulse oximetry also have demonstrated that deep and relatively prolonged variable decelerations occur often without any change in fetal oxygen saturation. Pregnancies complicated with decreased amniotic fluid (oligohydramnios) are associated with more frequent patterns of variable decelerations, and this is thought to be related to the loss of the protective effect of the amniotic fluid on the fetal umbilical cord. Such a relationship is further supported by the fact that, in cases with diminished amniotic fluid in labor treated with saline amnio-infusion via a transcervical catheter, there is a reduction in the frequency of variable decelerations in both preterm and term fetuses compared to controls [2]. Variable decelerations characteristically are very abrupt in onset and return to baseline. They may be associated with fetal movement or uterine contractions and are most commonly seen in the second stage of labor associated with maternal Valsalva and pushing efforts. Variable decelerations have different degrees of decrease of heart rate, time below baseline, and rate of return to baseline. The vast majority of variable decelerations are not associated with significant hypoxia or acidosis. Because of their frequency and unpredictability, variable decelerations must be evaluated and managed closely. With cord compression that is prolonged and repetitive, there may be the development of progressive fetal hypoxia and respiratory acidosis. Thus, variable decelerations have been graded as mild, moderate, and severe. Mild variable decelerations last for 2 min. Such a decrease must be 15 bpm below baseline and last 80% of fetuses in labor demonstrate at times Category II patterns [7]. Recently, specific management proposals for Category II tracings have been recommended and generally utilized [8]. These include the use of various algorithms for management depending upon the presence or absence of variability or accelerations of the fetal heart rate, the presence or absence of significant decelerations, the stage of labor, and evidence of normal progress in labor. 11. Conclusion The use of EFM continues to be ubiquitous in modern labor and delivery units. Whereas there is no clear consensus regarding strict guidelines for the clinical management of all patients using specific fetal heart rate patterns, there is little variation in opinion about the definition of distinctly normal and abnormal patterns. Most fetuses demonstrate patterns of heart rate during labor that are intermediate between these extremes. In such a setting, the specific clinical management and presumed fetal status are controversial and there is not one accepted standard of care for management. With such a background, it is imperative that clinical concerns regarding fetal or maternal status must be clearly documented and shared among all members of the health care team. This includes clear communication among the physicians and nurses managing the patient, as well as with the neonatal team tasked with caring for and at times emergently resuscitating the newborn. Whereas strides have been clearly made toward eliminating the cases of unexpected intrapartum stillbirth, the use of continuous EFM remains a challenge in the appropriate interpretation, application, and credentialing of those who utilize it in an effort to safeguard the mother and her fetus during the process of parturition.
Practice points EFM is a highly reliable assessment of normal fetal oxygenation when it is Category I. Over the course of labor, the fetal heart rate will often change between Categories I and II and does not necessarily suggest any significant worsening of fetal status. Category III fetal heart rate patterns are most concerning, correlate highly with need for neonatal resuscitation, and need to be acted upon with either improvement or delivery of the fetus.
Please cite this article in press as: Nageotte MP, Fetal heart rate monitoring, Seminars in Fetal & Neonatal Medicine (2015), http://dx.doi.org/ 10.1016/j.siny.2015.02.002
M.P. Nageotte / Seminars in Fetal & Neonatal Medicine xxx (2015) 1e5
5
References Research directions There needs to be ongoing research into new technologies that may serve as adjuncts to EFM for fetal assessment. Studies utilizing proposed management strategies for Category II tracing must be done to provide evidence that such strategies are appropriate. Use of a common language and intrapartum management approach must be stressed for each institution providing labor and delivery services, as well as monitoring to insure patient safety and improved perinatal outcomes.
Conflict of interest statement None declared. Funding sources
[1] Freeman RK. Intrapartum fetal monitoring e a disappointing story. N Engl J Med 1990;322:624e6. [2] Nageotte MP, Freeman RK, Garite TJ, Dorchester W. Prophylactic intrapartum amnioinfusion in patients with preterm premature rupture of membranes. Am J Obstet Gynecol 1985;153:557e62. [3] Hon EH. Observations on “pathologic” fetal bradycardia. Am J Obstet Gynecol 1959;77:1084e8. [4] Caldeyro-Bacia R, Casaciberta C, Bustos R, Giussi G, Gulin L, Escarcena L, et al. Correlation of intrapartum changes in fetal heart rate with fetal blood oxygen and acid base state. In: Adamsons K, editor. Diagnosis and treatment of fetal disorders. New York: Springer-Verlag; 1968. p. 205e25. [5] Murata Y, Miyake Y, Yamamoto T, Higuchi M, Hesser J, Ibara S, et al. Experimentally produced sinusoidal fetal heart rate pattern in the chronically instrumented fetal lamb. Am J Obstet Gynecol 1985;153:693e6. [6] Macones GA, Hankins GD, Spong CY, Hauth J, Moore T. 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;112:661e6. [7] American College of Obstetricians and Gynecologists. Management of intrapartum fetal heart rate tracings: ACOG practice bulletin no. 116. Obstet Gynecol 2010;116:1232e40. [8] Clark SL, Nageotte MP, Garite TJ, Freeman RK, Miller DA, Simpson KR, et al. Intrapartum management of category II fetal heart rate tracings: towards standardization of care. Am J Obstet Gynecol 2013;209:89e97.
None.
Please cite this article in press as: Nageotte MP, Fetal heart rate monitoring, Seminars in Fetal & Neonatal Medicine (2015), http://dx.doi.org/ 10.1016/j.siny.2015.02.002
