ABSTRACT
Introduction It has long been known that labor is a risk factor for fetal mortality and for neonatal morbidity and mortality. Through research carried out in the 1950s, 1960s, and early 1970s, obstetricians obtained a better understanding of fetal respiratory physiology and human fetal physiology in response to the labor process. It provided a basis for diagnostic techniques to detect possible fetal well-being and compromise. It was appreciated that clinical management could change fetal conditions. In 1961, Saling introduced intermittent scalp pH measurement as the first technique for direct assessment of fetal well-being during labor. 1 Fetal heart rate (FHR) monitoring technologies were developed in the 1950s and 1960s by Hammacher et al, 2 Hon and Quilligan, 3 Caldeyro-Barcia et al, 4 and others. By the late 1960s and early 1970s, equipment for intrapartum fetal evaluation was commercially available. In the 1970s, obstetricians had very optimistic expectations that, with intrapartum surveillance (utilizing continuous FHR monitoring and intermittent fetal scalp pH determinations), intrapartum stillbirths and neonatal neurological injuries caused by intrapartum hypoxia could be significantly reduced or eliminated. The hope was that with continuous electronic FHR monitoring, ‘early asphyxia ’ would be recognized; through timely obstetrical intervention, asphyxia-induced brain damage, or neonatal death, would be avoided. Continuous electronic fetal monitoring (EFM) was introduced into widespread clinical practice before evidence from randomized clinical trials demonstrated either efficacy or safety. In the 1970s and 1980s, continuous electronic FHR monitoring became routine in most hospitals in the United States and the Western world. During the last 30 years, thousands of articles have been written on this topic. Initial retrospective studies evaluated 135 000 patients and showed a more than three-fold improvement in the intrapartum fetal death rate for the electronically monitored group versus the control group with intermittent auscultation (IA). 5,6 Many randomized
routine continuous electronic fetal monitoring (EFM) with intermittent auscultation (IA) for intrapartum surveillance. Recently, there has been increasing utilization of central monitoring systems and computerized recognition and interpretation of fetal heart rate patterns. 7-11
Fetal heart rate patterns Over the past 40 years, many scientific articles have been written concerning the definitions of FHR patterns and recommendations for their interpretation. For many years there was confusion about terminology and definitions used to describe and interpret FHR patterns. In 1997, recommendations for research guidelines for the interpretation of fetal heart rate were published. 12 The recommendations resulted from a National Institute of Child Health and Human Development (NICHD) Research Planning Workshop that had the purpose to assess the research status of this area and publish research recommendations. 12 This consensus report suggested standardized and unambiguous definitions of FHR patterns for the purposes of improving research studies on the reliability and validity of FHR interpretation as well as studies of the relationship between FHR patterns and outcome. Four major parameters of FHR were defined: baseline rate, baseline FHR variability, accelerations, and decelerations (variable, early, late, and prolonged). The most recent American College of Obstetricians and Gynecologists (ACOG) Practice Bulletin published in 2005, entitled ‘Intrapartum Fetal Heart Rate Monitoring ’ , 13 included the NICHD Research Planning Workshop FHR pattern definitions and descriptions. 12
Baseline FHR baseline is the mean FHR over a given 10-minute period (rounded to the nearest 5 beats/min). The normal
defined as a decrease in FHR baseline below 110 beats/ minute for 10 minutes or longer. Mild degrees of bradycardia may occur in the second stage of labor, and often immediately before birth. The fetus is generally able to tolerate bradycardia by compensating with an increased stroke volume. However, this ability to compensate with increased stroke volume in response to bradycardia breaks down at severe decreases in FHR, below 60 beats/minute. Catastrophic events associated with bradycardia include umbilical cord prolapse, umbilical cord occlusion, or uterine rupture. Congenital heart block due to the presence of anti-Ro and/or anti-La antibodies from maternal collagen vascular disease may be another uncommon cause. 14 Tachycardia, a FHR baseline > 160 beats/min for 10 minutes or longer, may occur due to maternal pyrexia, medications ( β -sympathomimetics, cocaine), chorioamnionitis, fetal hypoxia, fetal anemia, or tachyarrythmias. In tachycardia there is increased sympathetic and/or decreased parasympathetic autonomic tone, which is associated with decreased FHR variability. Chronically instrumented fetal sheep exposed to umbilical cord occlusions for 1 minute every 2.5 minutes develop a fall in nadir of FHR decelerations and a rise in interocclusion fetal heart rate, or tachycardia, due to increased catecholamine activity. 15,16 Tachycardia, in cases of intrapartum acidemia, does not appear in isolation. If tachycardia is seen with normal FHR variability and no periodic changes, it should be assumed to be due to other causes.
