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Fetal acidemia is a common final pathway to fetal death, and in many cases, to fetal central nervous system injury. However, certain fetal pathophysiological processes are associated with significant category II or category III fetal heart rate changes before the development of or in the absence of fetal acidemia. The most frequent of these processes include fetal infection and/or inflammation, anemia, fetal congenital heart disease, and fetal central nervous system injury. In the presence of significant category II or category III fetal heart rate patterns, clinicians should consider the possibility of the aforementioned fetal processes depending on the clinical circumstances. The common characteristic of these pathophysiological processes is that their associated fetal heart rate patterns are linked to increased adverse neonatal outcomes despite the absence of acidemia at birth. Therefore, in these cases, the fetal heart rate patterns may provide more insight about the fetal condition and pathophysiology than the acid–base status at birth. In addition, as successful timing of intrapartum interventions on the basis of evolution of fetal heart rate patterns aims to prevent fetal acidemia, it may not be logical to continue to use the fetal acid–base status at birth as the gold standard outcome to determine the predictive ability of category II or III fetal heart rate patterns. A more reasonable approach may be to use the umbilical cord blood acid–base status at birth as the gold standard for determining the appropriateness of the timing of our interventions.
It is generally accepted that fetal acidemia is a common final pathway to fetal death and fetal central nervous system (CNS) injury. To improve the timely detection of fetal hypoxia and/or acidemia during labor, we recently described the evolution of the fetal heart rate (FHR) patterns of the deteriorating fetus and the “significant” category II patterns and proposed specific timings of our interventions to avoid fetal acidemia.
Decelerations, tachycardia, and decreased variability: have we overlooked the significance of longitudinal fetal heart rate changes for detecting intrapartum fetal hypoxia?.
Of course, the timing and progression of fetal deterioration would be expected to vary depending on the etiology of the deterioration and the extent of fetal reserves.
After extensive use of electronic fetal monitoring (EFM) in clinical practice, it is apparent that category II and even category III FHR patterns can be present when there is either no acidemia or long before the development of fetal acidemia. This concept implies that category II or III FHR patterns in certain situations may be better at providing potentially actionable information about the fetal condition and the in utero environment. Common situations where this can apply include fetal infection and/or inflammation, anemia, congenital heart disease, and fetal CNS injury.
The aims of this article are as follows: (1) to provide an overview of the most common fetal pathophysiologic processes associated with category II or III FHR patterns without fetal acidemia and discuss possible mechanisms that could explain the lack of abnormal acid–base status prediction (especially by category II FHR patterns); (2) to alert clinicians that category II or III FHR patterns may not necessarily be the result of primary uteroplacental insufficiency unmasked by uterine contractions during labor and that such FHR patterns could reflect a specific underlying fetal pathophysiologic process associated with adverse neonatal outcomes independent of fetal acidemia; (3) to provide evidence that category II or III FHR patterns may provide insightful information and outcome prediction about the fetus even before the development of fetal acidemia; and (4) to challenge the traditionally held belief that acid–base status should always be the “gold standard” outcome for assessing the clinical relevance of FHR patterns. As many of the articles that we will cite are from literature published before the 2008 Eunice Kennedy Shriver National Institute of Child Health and Human Development FHR pattern classification, we will describe the specific FHR changes by the language that the authors used.
Fetal infection and/or inflammation
In our experience, the most frequent pathophysiological process for category II or III FHR patterns, in the absence or long before the development of fetal acidemia, is fetal infection and/or inflammation. The classical clinical scenarios associated with in utero fetal infection and/or inflammation are preterm premature rupture of the membranes (PROM), preterm labor with intact membranes, and term labor with prolonged rupture of membranes. A less frequent scenario is “unexplained” decreased fetal movement in the absence of PROM or labor.
Fetal tachycardia has long been recognized as a clinical sign of infection. It is one of the generally accepted criteria for the diagnosis of maternal infection in patients with PROM (supporting the diagnosis of clinical chorioamnionitis), despite the fact that it represents fetal information.
have shown that in patients with PROM who subsequently develop infection (maternal and/or neonatal), the FHR reactivity diminishes before both the development of overt maternal infection and before the development of fetal acidemia from advanced fetal sepsis. Antepartum daily follow-up of prolonged PROM with nonstress testing demonstrated that nonreactive FHR testing 24–48 hours before delivery has an overall sensitivity, specificity, and positive and negative predictive values of 78.1%, 86.3%, 65.7%, and 92.1%, respectively (positive likelihood ratio, 5.7 and negative likelihood ratio, 0.2) for maternal and/or neonatal infection in the absence of maternal symptomatology and in the absence of fetal acidemia.
Gestational age has an impact on these measures. The aforementioned detection rates were 76.1%, 58.8%, 61.5%, and 80%, respectively (positive likelihood ratio, 1.8 and negative likelihood ratio, 0.4) for gestations 32 weeks or less and 81.8%, 95%, 75%, and 96.6%, respectively (positive likelihood ratio, 16.3 and negative likelihood ratio, 0.2) for gestations greater than 32 weeks.
The definition of a reactive nonstress test was 2 or more FHR accelerations at least 15 beats per minute (bpm) in amplitude and at least 15 seconds duration in a 20-minute period, regardless of the gestational age. The conversion of an initial reactive nonstress test to nonreactive on subsequent daily testing was associated with subsequent infection in 89.5% of the cases, whereas persistent nonreactive testing was associated with infection in 80% of the cases.
Importantly, there were no differences in the umbilical cord blood pH (mean±2 standard deviations) between the infected and noninfected cases (artery 7.29±0.14 vs 7.30±0.11, respectively; vein 7.34±0.11 vs 7.35±0.11, respectively). During the antepartum period and in early labor of PROM patients, the finding of a nonreactive FHR pattern was more common than fetal tachycardia in patients who eventually develop maternal or early neonatal sepsis.
In evaluating 197 patients with the clinical diagnosis of chorioamnionitis during labor, Wendel et al showed that the overwhelming majority of the fetuses exhibited abnormal FHR changes including fetal tachycardia (73%,), FHR nonreactivity (28%), absent variability (5%), late decelerations (4%) and severe variable decelerations (4%); despite the aforementioned FHR changes, none of the fetuses had pathologic acidemia (umbilical artery cord pH<7.00), and none of the FHR patterns was associated with umbilical cord artery pH <7.20 at birth.
by using computerized cardiotocography, found that patients who were later found to have histologic chorioamnionitis had higher baseline FHR, a higher number of low variation episodes, and lower short term variations than the control group, despite the lack of acidemia as determined by (median and interquartile) umbilical cord pH measurements (7.30 [7.24–7.35] vs 7.29 [7.25–7.35], respectively).
In addition to increased baseline FHR and decreased variability, severe variable decelerations have been associated with histologic evidence of acute inflammation in patients with preterm labor or preterm PROM in the absence of fetal acidemia.
reported on the FHR patterns within 24 hours of delivery in patients admitted at <32 weeks with preterm PROM or preterm labor with intact membranes. In addition to decreased FHR variability, severe FHR variable decelerations were directly related to acute amnionitis and acute umbilical vasculitis in the absence of fetal acidemia. The umbilical artery cord pH and base deficit measurements were normal in patients who had severe umbilical vasculitis (7.3±0.1 and −4.4±4.0, respectively) or severe amnionitis (7.30±0.09 and −4.2±4.0, respectively).
The authors concluded that severe FHR variable decelerations in these patients are related to histologic inflammation of the amnion and the umbilical cord. Sensitization of the umbilical artery smooth muscle by inflammatory mediators with their resultant vasoactive effects on the umbilical vasculature could be at least part of the explanation for the severe FHR variable decelerations as fetal acidemia was not present in these cases.
The mechanism by which infection causes FHR changes in the absence of fetal acidemia is not known. One speculation is that intra-amniotic or fetal infection and/or inflammation mediators may increase metabolism, and thus, fetal oxygen demands, leading to “relative” tissue hypoxia, resulting in compensatory tachycardia and even malfunction of the CNS centers that control FHR reactivity.
suggests that there are systemic, pulmonary, and hemodynamic changes that occur in response to fetal infection and/or inflammation associated with reduction in tissue oxygen delivery. This leads to progressive changes in the FHR patterns as noted above even before there are observed changes in the arterial pH and base excess. In the later stages of a systemic fetal inflammatory response, the tissue hypoxia becomes severe, resulting in anaerobic metabolism, cardiac dysfunction, and fetal acidemia.
To summarize the evidence, in women with preterm PROM or preterm labor with intact membranes, the presence of significant category II or III FHR patterns, including fetal tachycardia, increase in FHR baseline, decreased variability, and severe variable decelerations
Decelerations, tachycardia, and decreased variability: have we overlooked the significance of longitudinal fetal heart rate changes for detecting intrapartum fetal hypoxia?.
, should alert the clinician toward the strong possibility of intrauterine infection and/or inflammation rather than primary fetal acidemia. We, and others also, have found that fetal infection and/or inflammation is the most common cause for significant category II or category III FHR in women who present with preterm PROM, preterm labor, or term labor with prolonged rupture of membranes. The combination of such FHR patterns during labor and normal umbilical cord gases should always alert the clinician to the strong possibility of fetal infection and/or inflammation. These cases should also prompt a histologic evaluation of the placenta to confirm the presence or absence of infection and/or inflammation.
Fetal anemia
The classic clinical scenarios associated with fetal anemia include the presence of maternal red blood cell alloimmunization, fetomaternal hemorrhage, and fetal parvovirus B19 infection. Some patients may present with decreased or absent fetal movement. Existing evidence suggests that anemic fetuses, especially in cases of severe anemia, exhibit several FHR changes in the absence of or long before the development of acidemia. Mild degrees of fetal anemia are not associated with clinically appreciable FHR changes. However, severe fetal anemia is frequently associated with FHR changes, including the classic sinusoidal FHR pattern, which sometimes can be seen in primary fetal asphyxia or hypoxia, CNS injury, infection, cardiac anomalies, and in the presence of certain drugs, especially narcotics. The actual sinusoidal FHR pattern is rare. It has a stable baseline and is continuous or alternating with periods or a nonreactive FHR, decreased variability, and no accelerations.
Severe fetal anemia (fetal hemoglobin more than 7 standard deviations below normal for gestational age) can also be associated with lack of accelerations, decreased FHR reactivity, baseline tachycardia, and late or prolonged decelerations.
FHR monitoring before cordocentesis in the third trimester of red cell-immunized pregnancies has shown that severe fetal anemia is consistently associated with late decelerations and/or sinusoidal FHR patterns because of low hemoglobin or oxygen content rather than low partial pressure of oxygen (pO2) or pH of the fetus. Even with extreme degrees of fetal anemia, the pH, pO2, and partial pressure of carbon dioxide (pCO2) of the fetus usually remain within the normal ranges
In a third trimester study of fetuses where the FHR was studied before cordocentesis for red cell alloimmunization, it was found that a sinusoidal FHR pattern is observed only in cases with severe fetal anemia, whereas lesser degrees of anemia are associated with decreased FHR reactivity and baseline variability and also late FHR decelerations. The positive predictive value of these FHR changes for fetal anemia was 50% to 100% depending on the definition of the FHR abnormalities.
The aforementioned studies using cordocentesis and correlating FHR patterns with hemoglobin levels and fetal acid–base status provide strong evidence that these FHR patterns in fetal anemia are developed in the absence of fetal acidemia. This was confirmed in an observational study of 286 pretransfusion fetal blood samplings where umbilical venous blood gases, including pH, pCO2, pO2, base excess, and O2 saturation remained virtually unchanged, even in severe anemia cases; the mean (and range) umbilical vein pH was 7.36 (7.28–7.51), 7.36 (7.17–7.45), 7.38 (7.28–7.46), and 7.38 (7.29–7.43) in severe anemia with hydrops, severe anemia without hydrops, moderate anemia, and no anemia, respectively.
The mechanism of fetal anemia causing significant category II or category III FHR patterns in the absence of fetal acidemia is unknown. One speculation is that in fetal anemia cases, the presence of FHR changes is related to low fetal blood oxygen content rather than fetal acidemia, which results in tissue hypoxia and malfunction of fetal CNS centers.
Given the aforementioned evidence, clinicians should always consider the presence of fetal anemia in the presence of significant category II or category III FHR patterns, especially in the typical scenarios of patients with red cell isoimmunization, suspected fetal infection because of parvovirus B19 infection, or fetomaternal hemorrhage in patients presenting with unexplained reduced or absent fetal movement and normal fetal growth.
Fetal heart disease
Soon after the introduction of EFM in routine practice, it became obvious that nonhydropic fetuses with arrhythmias frequently exhibit aberrant FHR patterns in the absence of fetal acidemia. Sugarman et al
reported on the intrapartum FHR findings of term fetuses with atrial and ventricular premature contractions and supraventricular tachycardia, which included decreased FHR variability, moderate variable decelerations, and tachycardia. These fetuses were followed with fetal scalp pH during labor and umbilical cord and neonatal pH, pCO2, and base deficit. These measurements were normal in all cases, and no cases of congenital heart block or cardiac failure were seen among this group of fetuses.
Subsequent clinical experience showed that fetal heart disease including not only arrhythmias but also congenital heart disease in the absence of hydrops or heart failure can be associated with FHR changes in the absence of fetal acidemia.
In the presence of bradyarrhythmias or tachyarrhythmias, the most common FHR patterns are characterized by fetal bradycardia or tachycardia, respectively, frequently combined with minimal or absent FHR variability. Obstetrical definitions of fetal bradycardia and tachycardia are FHR<110 bpm and >160 bpm, respectively. However, in the presence of fetal bradyarrhthmias or tachyarrhythmias, the FHR typically deviates to a much greater extent below or above than the aforementioned cutoffs. Persistent fetal bradycardia, especially <100 bpm, in the presence of a normal biophysical profile, should raise suspicion about fetal arrhythmia. In fetuses with sinus and low atrial bradycardias, the FHRs range between 90 bpm and 110 bpm; lower FHRs should raise the suspicion of arrhythmias such as blocked atrial bigeminy, long QT syndrome, or atrioventricular block (AV) block. Extremely low FHR rates (<55–60 bpm) with minimal or absent FHR variability should raise the suspicion of an AV block.
An AV block is the result of maternal autoantibodies (SSA/Ro-mediated or SSB-La-mediated) in 45% to 48% of the cases, structural heart disease in 45% to 48% of the cases, and is idiopathic in 4% to 10% of the cases.
Fetal tachyarrhythmia should be suspected in the presence of sustained FHR>180 bpm. The most common etiology is supraventricular tachycardia, which is typically associated with FHR rates of 230 to 280 bpm.
These very low or very high FHRs, in the absence of hydrops or heart failure, are usually associated with normal fetal acid–base status. Hydrops or fetal heart failure can exhibit significant category II or category III FHR changes, including prolonged bradycardia, late decelerations, and minimal or absent FHR variability. In these cases, umbilical vein gases have almost normal values of pH, PCO2, and PO2, but acidotic pH with high PCO2 and low O2 values is observed in the umbilical artery.
Some authors have recommended monitoring serial scalp pH measurements during labor in the presence of significant arrhythmias or hydrops to confirm normal fetal pH and allow a vaginal delivery.
Given its limited association with acidemia, using fetal scalp pH in these circumstances for reassurance about fetal well-being does not seem likely to be clinically useful; in addition, scalp pH sampling is not currently used in the United States.
Fetal structural heart disease, even in the absence of arrhythmia, is associated with abnormal FHR patterns in the absence of fetal acidemia. A review of 116 cases of fetal heart disease showed that almost half of these fetuses develop aberrant FHR patterns in labor compared with 18% of controls, with the most prominent FHR abnormalities being severe variable and prolonged decelerations.
There was no difference between the study and control groups in the mean umbilical artery pH (7.29±0.09 vs 7.30±0.07, respectively) or the number of fetuses with pH ≤7.20 (10% vs 8%, respectively). Tetralogy of Fallot, isomerism, univentricular heart, pulmonary stenosis or atresia, and coarctation or interruption of the aortic arch were the major heart abnormalities associated with abnormal FHR patterns. Another more recent study of 134 fetuses with structural heart disease found that almost all of these fetuses had a normal umbilical artery pH at birth (mean pH [95% confidence interval], 7.20 [7.20–7.40] vs controls, 7.22 [7.21–7.24]), suggesting compensated circulation in utero. Only 2 fetuses had pathologic acidemia at birth (umbilical artery pH<7.00). Both of these fetuses developed recurrent late decelerations and minimal FHR variability during labor, but both had additional complications such as growth restriction and preeclampsia that may have explained their inability to tolerate labor.
In fetuses with structural heart disease without bradyarrhythmias or tachyarrhythmias, there may be several possible mechanisms implicated for the presence of FHR pattern changes in the absence of fetal acidemia. One possibility is placental dysfunction secondary to small placental size and vascular malperfusion, resulting in relative fetal hypoxemia.
Other possible mechanisms may be related to the type of the cardiac anomaly. For instance, in fetuses with isomerism and/or univentricular heart the mechanism may be related to an abnormality of the impulse conduction system because of aberrant laterality.
In fetuses with Tetralogy of Fallot, pulmonary stenosis or atresia, or coarctation of the aorta increased pressure in the right ventricle, if severe enough, may lead to right ventricle hypertrophy and elicit FHR changes. However, it is unknown if this increased overload of the right ventricle leads to FHR changes via an aberrant electrical conduction or via some other mechanism.
The association of significant category II or category III FHR patterns during labor, fetal acidemia at birth, and CNS injury has been well-documented.
whereas the remaining may suffer a preexisting injury before labor or in the neonatal period. Neurologic injury can be the result of insults during the antepartum, intrapartum, or neonatal period, including metabolic, genetic, vascular, hematologic, inflammatory, or transient hypoxic insults.
On admission to the Labor and Delivery, the clinician should be able to recognize FHR patterns compatible with preexisting neurologic injury (ie, absent FHR variability, severe bradycardia, or decelerations with absent or minimal variability, wandering baseline, sinusoidal, or sawtooth FHR patterns) and counsel the parents accordingly. However, many fetuses with preexisting CNS injury may present with subtle FHR changes, or they may even present with reassuring (reactive) FHR patterns. Many of these fetuses do not tolerate uterine contractions and almost always develop significant category II or category III FHR patterns during labor
Therefore, in this latter scenario, the intrapartum FHR patterns are more predictive of the adverse neurologic outcome for the baby than its acid–base status at birth.
reported on the association among intrapartum FHR patterns, fetal metabolic acidemia (umbilical artery pH <7.00 and base deficit ≥12 mmol/L) at birth, and neurologic injury in 58 high-risk cases delivered at ≥34 weeks gestation. In that study, there were 46 cases of neurologically damaged fetuses, 33 of which were cerebral palsy (CP). Of these 58 eligible cases, only 15 (26%) were associated with acidemia; the remaining 43 (74%) were not related to acidemia. Of those who were not acidemic at birth and demonstrated CNS injury, the overwhelming majority (26/35 or 74%) had significant category II or category III FHR patterns in labor, including bradycardias, prolonged decelerations, severe variable decelerations, recurrent late decelerations, and loss of FHR variability. These FHR patterns remained present even after excluding 3 cases with moderate acidemia (pH, 7.01–7.10) from the nonacidemia-related group. All 10 cases of CP related to acidemia had bradycardia (<80 bpm for ≥13 min) during labor. The detection rate of CNS injury was only 24% (11/46) by acidemia, whereas the detection rate by abnormal FHR patterns (category II and III) was 80% (37/46); the detection rate of CP was only 30% (10/33) by acidemia and 79% (26/33) by abnormal FHR patterns. These observations suggest the following: (1) the FHR patterns associated with fetal CNS injury are different in the acidemic (ie, severe bradycardia in CP cases) vs nonacidemic-related cases; (2) FHR tracing abnormalities have a stronger association with fetal CNS injury cases, and these abnormalities may have prompted interventions that would prevent fetal acidemia or fetal CNS injury by interrupting what would otherwise be progressive deterioration; (3) nonacidemia-related neurologic injuries may be frequently misdiagnosed as acidemia-related; and (4) category II or III FHR patterns may not necessarily cause CNS injury mediated by fetal acidemia but could be the result of preexisting injury or other mechanisms.
In another study from Sweden, which investigated the relationship among 80 cases of neonatal encephalopathy, intrapartum FHR patterns, and fetal acidemia at birth, it was found that asphyxia during labor (umbilical cord pH <7.00 and base deficit ≥12 mmol/L) was responsible for the injury in 48/80 (60%) of the cases, most of which evolved during labor (43/80 or 54%).
Neonatal encephalopathy and neonatal death rates were more frequent with an abnormal rather than with a normal admission cardiotocography (CTG) pattern (45% vs 22% and 21% vs 6%, respectively).
Abnormal FHR patterns included late FHR decelerations and decreased variability. An abnormal CTG on admission had a detection rate of subsequent development of neonatal encephalopathy of 36% (29/80), which increased to 87% (70/80) when labor FHR pattern evolution was considered. This is in contrast to the lower detection rate of neonatal encephalopathy by acidemia at birth of 60% (48/80).
A nationwide cohort study from Japan, which studied the FHR patterns during labor of 1069 consecutive CP cases born at or beyond 34 weeks gestation, found that abnormal FHR patterns on admission (bradycardia or persistently decreased or minimal FHR variability) had a detection rate of CP of 30% (316/1069), which increased to 80% (857/1069) when abnormal FHR pattern evolution during labor was considered.
In contrast, fetal acidemia at birth, as defined by umbilical artery pH <7.00, detected only 38% (304/793) of the CP cases with available pH and 46% (341/733) of the CP cases with available umbilical artery base deficit (12 mEq/L or more).
The findings of the above studies suggest that infants without metabolic acidemia and with findings of hypoxia-ischemia in neuroimaging at birth may have had intrauterine recovery of any acid–base abnormality before birth or local CNS insult without systemic acid–base disturbance. In either case, it appears that the FHR patterns seem to be more sensitive in the prediction of CNS injury in general or CP than fetal acidemia or metabolic fetal acidemia (Table 1). The speculation regarding the mechanism for abnormal FHR patterns in the presence of CNS injury is related to the influence of the ischemic injury on the cardioregulatory regions in the brain stem, posterior hypothalamus, and medulla oblongata, which control cardiac activity through the autonomic nervous system.
Table 1Detection rates of central nervous system injury
In this article, we have described a variety of fetal pathophysiological processes with their associated FHR patterns and mechanisms, which provide useful information regarding the fetal condition before the development of fetal acidemia (Table 2). Figure 1, Figure 2, Figure 3, Figure 4, Figure 5 illustrate examples of FHR tracings from each of the aforementioned fetal pathophysiological processes. These examples and the reviewed evidence indicate that FHR patterns may provide more insightful information with respect to timing interventions and may therefore be more important than the acid–base status. Although fetal acid–base status remains an important measure of the fetal condition at birth, we conclude that using fetal acid–base as a gold standard to determine the predictive ability of FHR patterns has significant limitations. It appears that FHR patterns may be more informative of the fetal condition than fetal acid–base status. The best use of acid–base status at birth may be in determining the appropriateness of the timing of our interventions.
Table 2Fetal pathophysiological processes and possible mechanisms for fetal heart rate abnormalities in the absence of fetal acidemia
Fetal pathophysiological process
Fetal heart rate changes and patterns
Possible pathophysiological mechanism(s)
1. Infection and/or inflammation
Tachycardia (>160 bpm); increasing FHR baseline; decreased, minimal, or absent baseline variability; change from reactive to nonreactive pattern; severe variable decelerations, sinusoidal; high rate of low variation episodes, and lower short- term variations on cCTG
Increased fetal metabolism, and thus, fetal oxygen demands, leading to relative tissue hypoxia and malfunction of CNS centers; systemic hemodynamic and circulatory changes leading to reduction in tissue oxygen delivery; inflammation of umbilical and chorionic vessels leading to vasoconstriction and even cardiac dysfunction
2. Anemia
Sinusoidal pattern; nonreactive pattern; decreased baseline variability; tachycardia, late decelerations, or prolonged decelerations
Low fetal blood oxygen content resulting in tissue hypoxia and malfunction of CNS centers that control fetal heart rate
3. Congenital heart disease a. Arrhythmias b. Structural disease
a. Decreased or absent baseline variability; variable decelerations; bradycardia <100 bpm (bradyarrhthmias); tachycardia >180 bpm (tachyarrhthmias) b. Severe variable decelerations, prolonged decelerations, recurrent late decelerations, or minimal variability
a. Arrhythmias: intrinsic cardiac rhythm disturbance because of bradyarrhthmias or tachyarrhthmias b. Structural disease: placental vascular malperfusion; abnormalities in the impulse conduction system; and increased pressure in ventricles leading to overload, hypertrophy, and aberrant electrical conduction
4. CNS injury
Absent or minimal variability; severe bradycardia or decelerations with minimal or absent variability; sinusoidal, sawtooth, or wandering baseline patterns
Prelabor or nonacidemia-related injury affecting the cardioregulatory regions in the brain stem, posterior hypothalamus, and medulla oblongata
bpm, beats per minute; cCTG, continuous cardiotocography; CNS, central nervous system; FHR, fetal heart rate.
Vintzileos. Fetal heart rate patterns vs fetal acidemia. Am J Obstet Gynecol 2022.
This patient was at 35 weeks and 5 days gestation in active labor; on admission, there were frequent uterine contractions accompanied by late FHR decelerations (arrows) (A); 60 min after admission, persistent and frequent late decelerations (arrows) with absent FHR variability were noted, resulting in an undulating FHR pattern (B); 90 min after admission, persistent fetal tachycardia, absent variability, and subtle late decelerations (arrows) were noted (C). At cesarean delivery, 90 min after admission, foul smelling amniotic fluid was noted; Apgar scores were 1, 6, and 7 at 1, 5, and 10 minutes, respectively; cord artery pH=7.18, cord vein pH=7.21; neonatal blood cultures were positive for Listeria monocytogenes; the female neonate was treated for neonatal sepsis with gentamycin and ampicillin for 2 weeks. Paper speed 3 cm/min.
FHR, fetal heart rate.
Vintzileos. Fetal heart rate patterns vs fetal acidemia. Am J Obstet Gynecol 2022.
This patient was at 35 weeks and 5 days gestation in active labor; on admission, there were frequent uterine contractions accompanied by late FHR decelerations (arrows) (A); 60 min after admission, persistent and frequent late decelerations (arrows) with absent FHR variability were noted, resulting in an undulating FHR pattern (B); 90 min after admission, persistent fetal tachycardia, absent variability, and subtle late decelerations (arrows) were noted (C). At cesarean delivery, 90 min after admission, foul smelling amniotic fluid was noted; Apgar scores were 1, 6, and 7 at 1, 5, and 10 minutes, respectively; cord artery pH=7.18, cord vein pH=7.21; neonatal blood cultures were positive for Listeria monocytogenes; the female neonate was treated for neonatal sepsis with gentamycin and ampicillin for 2 weeks. Paper speed 3 cm/min.
FHR, fetal heart rate.
Vintzileos. Fetal heart rate patterns vs fetal acidemia. Am J Obstet Gynecol 2022.
This patient was at 25 weeks and 3 days gestation and complained of PROM; on admission, there was normal baseline FHR, moderate FHR variability, and no decelerations (A); 9 days after admission, at 26 weeks and 5 days gestation, uterine contractions, absent FHR variability, and occasional variable decelerations (arrow) were noted (B); before cesarean delivery, the fetus continued to exhibit absent FHR variability; in addition, the fetus had developed tachycardia at 180 beats per minute with moderate and severe variable decelerations (arrows) (C). Apgar scores were 1, 5, and 10 at 1, 5 and 10 min, respectively; cord artery pH=7.20, cord vein pH=7.26; the male neonate developed neutropenia and was treated for probable sepsis; placenta pathology revealed stage III, grade 2, necrotizing chorioamnionitis and funisitis (stage II, grade 2, severe umbilical arteritis and phlebitis). Paper speed 3 cm/min.
FHR, fetal heart rate; PROM, premature rupture of membranes.
Vintzileos. Fetal heart rate patterns vs fetal acidemia. Am J Obstet Gynecol 2022.
This patient was at 32 weeks gestation and complained of pelvic pressure and labor; on admission, the fetal heart race tracing had minimal variability and recurrent subtle late decelerations (arrows) (A); later on, the FHR pattern exhibited periods of “moderate” FHR variability but only associated with contractions resembling sinusoidal-like appearance (arrows) (B); then, absent baseline FHR variability and alternating between sinusoidal-like variability during contractions (black arrow) and late decelerations (blue arrow) (C). Cesarean delivery of a male infant, Apgar scores 4 and 7 at 1 and 5 minutes, respectively; cord artery pH=7.17, cord vein pH=7.20; neonate had severe anemia (hemoglobin=5 g/dL, hematocrit=18%) because of FMH hemorrhage and received several blood transfusions. Paper speed 3 cm/min.
This patient was at 32 weeks gestation and complained of pelvic pressure and labor; on admission, the fetal heart race tracing had minimal variability and recurrent subtle late decelerations (arrows) (A); later on, the FHR pattern exhibited periods of “moderate” FHR variability but only associated with contractions resembling sinusoidal-like appearance (arrows) (B); then, absent baseline FHR variability and alternating between sinusoidal-like variability during contractions (black arrow) and late decelerations (blue arrow) (C). Cesarean delivery of a male infant, Apgar scores 4 and 7 at 1 and 5 minutes, respectively; cord artery pH=7.17, cord vein pH=7.20; neonate had severe anemia (hemoglobin=5 g/dL, hematocrit=18%) because of FMH hemorrhage and received several blood transfusions. Paper speed 3 cm/min.
This patient was admitted in labor at 39 weeks gestation; on admission, the FHR tracing was category I, but 2 hours later, an abrupt onset of fetal tachycardia (arrow) with an unstable baseline was noted (arrow) (A); this episode of fetal tachycardia lasted approximately 1 hour (B) and was followed by periods of return to baseline, minimal variability, subtle decelerations (white arrows), and recurrent episodes of abrupt tachycardia (blue arrow) (C). Spontaneous vaginal delivery, Apgar scores 9 and 9 at 1 and 5 minutes; cord artery pH=7.28, cord vein pH=7.33; multiple episodes of sinus tachycardia with supraventricular ectopy on Holter monitoring; echocardiogram showed aneurysmal atrial septum with patent foramen ovale and small left to right shunt present; to be followed by pediatric cardiology. Paper speed 3 cm/min.
FHR, fetal heart rate.
Vintzileos. Fetal heart rate patterns vs fetal acidemia. Am J Obstet Gynecol 2022.
This patient was admitted in early labor at 39 weeks gestation with category I FHR tracings with moderate FHR variability and accelerations (arrows) (A); approximately 12 hours after admission when the patient entered active labor with category I FHR tracing, an abrupt onset of fetal tachycardia was noted (arrow); at that time, the cervical dilatation was 5 cm (B); this FHR change was followed by episodes of sawtooth FHR pattern (arrows) and persistent tachycardia with unstable FHR baseline; at that time, the patient was at 7 cm (C); approximately 3 hours later, the FHR pattern recovered to category I before pushing (D); during second stage pushing, the FHR pattern once again developed sawtooth episodes (black arrows), tachycardia with an unstable baseline, and decelerations (blue arrows); the tachycardia, decelerations (blue arrows), unstable baseline, and sawtooth episodes (E); this FHR pattern, including decelerations (blue arrows) and sawtooth episodes (black arrows), persisted until delivery (F). Normal spontaneous vaginal delivery, Apgar scores 9 and 9 at 1 and 5 minutes; cord gases were not taken; the baby was admitted to regular nursery; at 24 hours of life the neonate developed facial twitches, and an MRI the following day showed infarction of the left cerebral hemisphere because of middle cerebral artery occlusion, possible thrombosis; the MRI-based timing of the fetal stroke coincided with the abrupt onset of the FHR pattern abnormalities during labor. Paper speed 3 cm/min.
CNS, central nervous system; FHR, fetal heart rate; MRI, magnetic resonance imaging.
Vintzileos. Fetal heart rate patterns vs fetal acidemia. Am J Obstet Gynecol 2022.
This patient was admitted in early labor at 39 weeks gestation with category I FHR tracings with moderate FHR variability and accelerations (arrows) (A); approximately 12 hours after admission when the patient entered active labor with category I FHR tracing, an abrupt onset of fetal tachycardia was noted (arrow); at that time, the cervical dilatation was 5 cm (B); this FHR change was followed by episodes of sawtooth FHR pattern (arrows) and persistent tachycardia with unstable FHR baseline; at that time, the patient was at 7 cm (C); approximately 3 hours later, the FHR pattern recovered to category I before pushing (D); during second stage pushing, the FHR pattern once again developed sawtooth episodes (black arrows), tachycardia with an unstable baseline, and decelerations (blue arrows); the tachycardia, decelerations (blue arrows), unstable baseline, and sawtooth episodes (E); this FHR pattern, including decelerations (blue arrows) and sawtooth episodes (black arrows), persisted until delivery (F). Normal spontaneous vaginal delivery, Apgar scores 9 and 9 at 1 and 5 minutes; cord gases were not taken; the baby was admitted to regular nursery; at 24 hours of life the neonate developed facial twitches, and an MRI the following day showed infarction of the left cerebral hemisphere because of middle cerebral artery occlusion, possible thrombosis; the MRI-based timing of the fetal stroke coincided with the abrupt onset of the FHR pattern abnormalities during labor. Paper speed 3 cm/min.
CNS, central nervous system; FHR, fetal heart rate; MRI, magnetic resonance imaging.
Vintzileos. Fetal heart rate patterns vs fetal acidemia. Am J Obstet Gynecol 2022.
This patient was admitted in early labor at 39 weeks gestation with category I FHR tracings with moderate FHR variability and accelerations (arrows) (A); approximately 12 hours after admission when the patient entered active labor with category I FHR tracing, an abrupt onset of fetal tachycardia was noted (arrow); at that time, the cervical dilatation was 5 cm (B); this FHR change was followed by episodes of sawtooth FHR pattern (arrows) and persistent tachycardia with unstable FHR baseline; at that time, the patient was at 7 cm (C); approximately 3 hours later, the FHR pattern recovered to category I before pushing (D); during second stage pushing, the FHR pattern once again developed sawtooth episodes (black arrows), tachycardia with an unstable baseline, and decelerations (blue arrows); the tachycardia, decelerations (blue arrows), unstable baseline, and sawtooth episodes (E); this FHR pattern, including decelerations (blue arrows) and sawtooth episodes (black arrows), persisted until delivery (F). Normal spontaneous vaginal delivery, Apgar scores 9 and 9 at 1 and 5 minutes; cord gases were not taken; the baby was admitted to regular nursery; at 24 hours of life the neonate developed facial twitches, and an MRI the following day showed infarction of the left cerebral hemisphere because of middle cerebral artery occlusion, possible thrombosis; the MRI-based timing of the fetal stroke coincided with the abrupt onset of the FHR pattern abnormalities during labor. Paper speed 3 cm/min.
CNS, central nervous system; FHR, fetal heart rate; MRI, magnetic resonance imaging.
Vintzileos. Fetal heart rate patterns vs fetal acidemia. Am J Obstet Gynecol 2022.
Vintzileos. Fetal heart rate patterns vs fetal acidemia. Am J Obstet Gynecol 2022.
References
Vintzileos A.M.
Smulian J.C.
Decelerations, tachycardia, and decreased variability: have we overlooked the significance of longitudinal fetal heart rate changes for detecting intrapartum fetal hypoxia?.
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