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Intrapartum fetal atrial bigeminy — Diagnostic and therapeutic role of the fetal scalp stimulation test
Intrapartum fetal atrial bigeminy Diagnostic and therapeutic role of the fetal scalp stimulation test Joseph R. Wax, MD, Melissa Emmerich, MD, and M.K. Eggleston, Jr., MD Portsmouth, Virginia Concern for fetal hypoxia often leads to cesarean delivery when persistent fetal bradycardia is identified. A fetus with premature atrial contractions had a prolonged second-stage heart rate of 80 beats/min. Intrapartum echocardiography and electronic fetal heart rate monitoring distinguished bradycardia caused by blocked atrial bigeminy from hypoxic bradycardia. The fetal scalp stimulation test documented normal acid-base balance and normalized the ventricular rate, avoiding cesarean delivery. (AM J OBSTETGYNECOL 1996;174:1649-50.)
Key words: Fetal echocardiography, electronic fetal heart rate monitoring, fetal bradycardia, fetal scalp stimulation test
Persistent fetal bradycardia may be associated with hypoxia and acidosis and therefore often leads to cesarean delivery. The significance of bradycardia resulting from a fetal arrhythmia is variable and may be difficult to establish. Simultaneous intrapartum echocardiography and Doppler heart rate monitoring have demonstrated fetal well-being and avoided cesarean delivery in cases of congenital atrioventricular block) We present a fetus with premature atrial contractions who subsequently had second-stage bradycardia. Echocardiography and direct electronic fetal heart rate (FHR) monitoring diagnosed blocked atrial bigeminy. The fetal scalp stimulation tesff documented normal acid-base balance and corrected the ventricular rate, avoiding cesarean delivery.
Case report A 26-year-old primigravid woman was referred at 38 weeks' gestation for an irregular FHR detected by auscultation. The patient was otherwise healthy and had an unremarkable prenatal course. An obstetric sonogram showed a single living fetus with appropriate biometry, normal anatomy, normal amniotic fluid volume, and no evidence of hydrops. Fetal echocardiography detected no structural anomaly. M-mode ultrasonography showed that the irregular heart rhythm resulted from premature atrial contractions. Oxytocin induction of labor was offered to the patient by the referring physician and accepted.
From the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Naval Medical Center The opinions expressed in this article are those of the authors and do not necessarily reflect those of the Department of the Navy, the Department of Defense, or the United States government. Receivedfor publication October23, 1995; revised November 16, 1995; accepted December 28, 1995. Reprints not available from the authors. 6/1/71593
Intraparmm electronic FHR monitoring was conducted by scalp electrode. In spite of the arrhythmia, the heart rate was reactive with a baseline of 150 to 160 beats/min and no decelerations. As the patient entered the second stage of labor, the monitor recorded a heart rate of 80 beats/min. The bradycardia did not respond to maternal positioning and the patient remained normotensive. During a vaginal examination that ruled out umbilical cord prolapse, the FHR immediately returned to baseline and exhibited a 60-second acceleration of 30 beats/min above baseline (Fig. 1). When the heart rate decreased to 80 beats/rain on two later occasions, simultaneous real time ultrason0graphy and direct electronic monitoring showed atrial bigeminy with 2:1 conduction. Transcervical scalp stimulation caused the ventricular rate to return to 160 beats/min in each instance. After a 60-minute second stage, a 3650 gm female infant with 1- and 5-minute Apgar scores of 9 and 10, respectively, was spontaneously delivered. Physical examination was normal, and an electrocardiogram showed unifocal premature atrial contractions. Arterial cord blood gas values were pH 7.30, Pco9 46 m m Hg, Po216 mm Hg, bicarbonate 23 mmol/L, and base excess -3.1 mmol/L. At discharge on the second day of life the infant remained asymptomatic and the premature atrial beats had resolved.
Comment Prolonged and severe fetal bradycardia is often considered a sign of fetal hypoxia. If no reversible cause is found and no response to resuscitative measures is observed, cesarean delivery may be indicated. Our patient did not demonstrate any of the common causes of second-stage bradycardia, such as hypotension, cord compression, or cord prolapse. Because a fetal arrhythmia was present and labor was progressing rapidly, we sought to further 1649
1650 Wax, Emmerich, and Eggleston
May 1996 AmJ ObstetOynecol
Fig. 1. Real time ultrasonography showed feral bradycardia of 80 beats per minute (largearrows) to result from blocked atrial bigeminy. Fetal scalp stimulation (large arrowheads) resulted in controlled ventricular rate and FHR acceleration (small arrows). investigate the cause of the bradycardia and fetal acidbase status. Kleinman et al. 1 described the intrapartum use of Mmode ultrasonography and Doppler FHR recording to monitor fetuses with congenital atrioventricular block. The authors used these modalities to differentiate bradycardia caused by hypoxia from bradycardia caused by altered conduction. In contrast to that report, we did not use atrial reactivity as an indicator of fetal well-being because an atrial arrhythmia was present. These investigators additionally recommended the adjunctive use of scalp blood sampling to monitor acid-base status of the bradycardic fetus when labor is permitted) Fetal scalp blood sampling has been used to confirm the presence or absence of acidosis in the presence of a nonreassuring FHR pattern, An alternative procedure used in our case, the fetal scalp stimulation test, is noninvasive and requires no special equipment. The stimulation apparently detects an intact biophysical response under stress rather than the biochemical estimation of that stress offered by blood sampling.2 When the fetal reaction to stimulation demonstrated normal acid-base balance, labor continued, culminating in vaginal delivery. Scalp stimulation in our case consistently normalized the ventricular rate during episodes of blocked atrial bigeminy. Typically, the heart rate is governed by the
fastest intrinsic pacemaker. We hypothesize that the sympathetic response to scalp stimulation triggered the sinoatrial node to fire more rapidly than the rate of the ectopic focus, thereby recapturing control of the ventricular rate. Had the ventricular rate not responded in this manner, it is conceivable that a persistent bradycardia may have led to fetal acidosis. Under these circumstances, fetal scalp blood analysis or cesarean delivery would have been considered. In summary, fetal premature atrial contractions may be associated with blocked atrial bigeminy. Persistent bradycardia in this setting may not be related to hypoxia and therefore warrants further evaluation. We conclude that intrapartum scalp stimulation may confirm normal acidbase status while promoting a normal ventricular rate in the uncompromised fetus with blocked atrial bigeminy. When reassuring fetal status can be demonstrated, cesarean delivery may be avoided. REFERENCES
1. Kleinman CS, CopelJA, HobbinsJC. Combined echocardiographic and Doppler assessment of feral congenital atrioventricular block. BrJ Obstet Gynaecol 1987;94:967-74. 2. Clark SL, GimovskyML, Miller FC. The scalp stimulation test: a clinical alternative to fetal scalp blood sampling. AMJ OBS~T GYNECOL 1984;148:274-7.
Key words: Fetal echocardiography, electronic fetal heart rate monitoring, fetal bradycardia, fetal scalp stimulation test
Persistent fetal bradycardia may be associated with hypoxia and acidosis and therefore often leads to cesarean delivery. The significance of bradycardia resulting from a fetal arrhythmia is variable and may be difficult to establish. Simultaneous intrapartum echocardiography and Doppler heart rate monitoring have demonstrated fetal well-being and avoided cesarean delivery in cases of congenital atrioventricular block) We present a fetus with premature atrial contractions who subsequently had second-stage bradycardia. Echocardiography and direct electronic fetal heart rate (FHR) monitoring diagnosed blocked atrial bigeminy. The fetal scalp stimulation tesff documented normal acid-base balance and corrected the ventricular rate, avoiding cesarean delivery.
Case report A 26-year-old primigravid woman was referred at 38 weeks' gestation for an irregular FHR detected by auscultation. The patient was otherwise healthy and had an unremarkable prenatal course. An obstetric sonogram showed a single living fetus with appropriate biometry, normal anatomy, normal amniotic fluid volume, and no evidence of hydrops. Fetal echocardiography detected no structural anomaly. M-mode ultrasonography showed that the irregular heart rhythm resulted from premature atrial contractions. Oxytocin induction of labor was offered to the patient by the referring physician and accepted.
From the Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Naval Medical Center The opinions expressed in this article are those of the authors and do not necessarily reflect those of the Department of the Navy, the Department of Defense, or the United States government. Receivedfor publication October23, 1995; revised November 16, 1995; accepted December 28, 1995. Reprints not available from the authors. 6/1/71593
Intraparmm electronic FHR monitoring was conducted by scalp electrode. In spite of the arrhythmia, the heart rate was reactive with a baseline of 150 to 160 beats/min and no decelerations. As the patient entered the second stage of labor, the monitor recorded a heart rate of 80 beats/min. The bradycardia did not respond to maternal positioning and the patient remained normotensive. During a vaginal examination that ruled out umbilical cord prolapse, the FHR immediately returned to baseline and exhibited a 60-second acceleration of 30 beats/min above baseline (Fig. 1). When the heart rate decreased to 80 beats/rain on two later occasions, simultaneous real time ultrason0graphy and direct electronic monitoring showed atrial bigeminy with 2:1 conduction. Transcervical scalp stimulation caused the ventricular rate to return to 160 beats/min in each instance. After a 60-minute second stage, a 3650 gm female infant with 1- and 5-minute Apgar scores of 9 and 10, respectively, was spontaneously delivered. Physical examination was normal, and an electrocardiogram showed unifocal premature atrial contractions. Arterial cord blood gas values were pH 7.30, Pco9 46 m m Hg, Po216 mm Hg, bicarbonate 23 mmol/L, and base excess -3.1 mmol/L. At discharge on the second day of life the infant remained asymptomatic and the premature atrial beats had resolved.
Comment Prolonged and severe fetal bradycardia is often considered a sign of fetal hypoxia. If no reversible cause is found and no response to resuscitative measures is observed, cesarean delivery may be indicated. Our patient did not demonstrate any of the common causes of second-stage bradycardia, such as hypotension, cord compression, or cord prolapse. Because a fetal arrhythmia was present and labor was progressing rapidly, we sought to further 1649
1650 Wax, Emmerich, and Eggleston
May 1996 AmJ ObstetOynecol
Fig. 1. Real time ultrasonography showed feral bradycardia of 80 beats per minute (largearrows) to result from blocked atrial bigeminy. Fetal scalp stimulation (large arrowheads) resulted in controlled ventricular rate and FHR acceleration (small arrows). investigate the cause of the bradycardia and fetal acidbase status. Kleinman et al. 1 described the intrapartum use of Mmode ultrasonography and Doppler FHR recording to monitor fetuses with congenital atrioventricular block. The authors used these modalities to differentiate bradycardia caused by hypoxia from bradycardia caused by altered conduction. In contrast to that report, we did not use atrial reactivity as an indicator of fetal well-being because an atrial arrhythmia was present. These investigators additionally recommended the adjunctive use of scalp blood sampling to monitor acid-base status of the bradycardic fetus when labor is permitted) Fetal scalp blood sampling has been used to confirm the presence or absence of acidosis in the presence of a nonreassuring FHR pattern, An alternative procedure used in our case, the fetal scalp stimulation test, is noninvasive and requires no special equipment. The stimulation apparently detects an intact biophysical response under stress rather than the biochemical estimation of that stress offered by blood sampling.2 When the fetal reaction to stimulation demonstrated normal acid-base balance, labor continued, culminating in vaginal delivery. Scalp stimulation in our case consistently normalized the ventricular rate during episodes of blocked atrial bigeminy. Typically, the heart rate is governed by the
fastest intrinsic pacemaker. We hypothesize that the sympathetic response to scalp stimulation triggered the sinoatrial node to fire more rapidly than the rate of the ectopic focus, thereby recapturing control of the ventricular rate. Had the ventricular rate not responded in this manner, it is conceivable that a persistent bradycardia may have led to fetal acidosis. Under these circumstances, fetal scalp blood analysis or cesarean delivery would have been considered. In summary, fetal premature atrial contractions may be associated with blocked atrial bigeminy. Persistent bradycardia in this setting may not be related to hypoxia and therefore warrants further evaluation. We conclude that intrapartum scalp stimulation may confirm normal acidbase status while promoting a normal ventricular rate in the uncompromised fetus with blocked atrial bigeminy. When reassuring fetal status can be demonstrated, cesarean delivery may be avoided. REFERENCES
1. Kleinman CS, CopelJA, HobbinsJC. Combined echocardiographic and Doppler assessment of feral congenital atrioventricular block. BrJ Obstet Gynaecol 1987;94:967-74. 2. Clark SL, GimovskyML, Miller FC. The scalp stimulation test: a clinical alternative to fetal scalp blood sampling. AMJ OBS~T GYNECOL 1984;148:274-7.