Case Study—Primary Care

Bradycardia in a Term Newborn Janice F. Ballou, MSN, APRN, BC, PNP, Barbara P. Gray, PhD, RN, CPNP, & Peggy Mancuso, PhD, CNM, RN

KEY WORDS Bradycardia, vagal innervation, parasympathetic control

A reportedly healthy Hispanic male infant was scheduled for a routine discharge examination at 52 hours of life from a newborn nursery. The infant had been roomSection Editors Jo Ann Serota, DNP, CPNP, FAANP Corresponding Editor Ambler Pediatrics Ambler, Pennsylvania Beverly Giordano, MS, RN, CPNP, PMHS Department of General Pediatrics/ADHD University of Florida, Gainesville Gainesville, Florida Donna Hallas, PhD, PNP-BC, CPNP, PMHS, FAANP New York University College of Nursing New York, New York Janice F. Ballou, Pediatric Nurse Practitioner, Newborn Nursery, Parkland Health & Hospital System, Dallas, TX, and Doctorate of Nursing Practice Student, Texas Woman’s University, Dallas, TX. Barbara P. Gray, PNP Program Coordinator, Texas Woman’s University, Dallas, TX. Peggy Mancuso, DNP Coordinator, Texas Woman’s University, Dallas, TX. Conflicts of interest: None to report. Correspondence: Janice F. Ballou, MSN, APRN, BC, PNP, 13768 Stirrup Ct, Forney, TX 75126; e-mail: [email protected] J Pediatr Health Care. (2014) -, ---. 0891-5245/$36.00 Copyright Q 2014 by the National Association of Pediatric Nurse Practitioners. Published by Elsevier Inc. All rights reserved.

ing in with his mother since 4 hours of life and was exclusively breastfeeding. His mother verbalized no concerns and was prepared to take the baby home. CASE PRESENTATION The infant’s medical history was significant for a spontaneous vaginal delivery to a 37-year-old gravida 4, para 4 woman, who had a history of gestational diabetes controlled by diet. One hour before delivery, meconium was noted in the amniotic fluid after artificial rupture of the membranes. No intrauterine exposure to medications occurred, and the mother denied use of recreational drugs, alcohol, or tobacco. A review of her electronic medical record revealed negative results of tests for human immunodeficiency virus, syphilis, and hepatitis B. Her previous three pregnancies and deliveries were uneventful. There was no family history of cardiac or autoimmune diseases. The infant’s family consisted of his 37-year-old mother, 39-year-old father, 12- and 3-year-old sisters, and 7-year-old brother. His father was employed in construction, and his mother did not work outside the home; neither parent completed high school. Spanish was their preferred language. The infant’s mother and father had a large network of extended family. A pediatrician attended the delivery because of the risk of neonatal hypoglycemia and the risk of respiratory depression because of the presence of meconium. The baby was vigorous at birth with a lusty cry and no signs of hypoglycemia or meconium aspiration. He immediately was placed across his mother’s bare chest and covered with warm blankets. The Apgar scores were 9 and 9 at 1 and 5 minutes, respectively. The baby fed for 5 to 10 minutes on each breast at approximately 1 hour of life. At 2 hours of life, he was transferred to a newborn nursery for assessment while his mother was transferred to a postpartum floor. The infant’s vital signs and laboratory evaluations are listed in Table 1, and the nurse’s assessment and routine medications are listed in Table 2. -/- 2014


TABLE 1. Vital signs and laboratory evaluations Time since birth 30 min 60 min 90 min 120 min 150 min Birth 36 hr

Temperature 36.4 C 37.1 C 36.8 C 36.5 C 36.7 C Umbilical cord pH Newborn Screen

Heart rate (bpm) Respiratory ratea Blood glucose (milligrams per deciliter)b Hematocritc 136 120 132 128 128 7.25d Normal

60 42 50 56 42

68 – 75 – 63

– – – – 57.7%/59.7%

Note. Heart rate and respiratory rate were measured over a 1-minute count. bpm = beats per minute. a Normal respiratory rate is 40 to 60 breaths per minute. b Normal blood glucose value is greater than 40 mg per deciliter. c Normal hematocrit value is between 40% and 60%. d Less than 7.0 indicates a risk for intrapartum anoxia (Thilo & Rosenberg, 2012).

At 8½ hours of life, the infant had an initial examination in his mother’s room. His heart rate (HR) was in the 130s with a regular rate and rhythm, and no murmurs were appreciated. Respirations were unlabored at 42 breaths per minute. The remainder of the examination was unremarkable. An interim examination completed at 32 hours of life was normal except for the finding of a short tongue frenulum, or mild ankyloglossia. A lactation consultant and speech therapist evaluated the baby using the Hazelbaker Assessment Tool for Lingual Frenulum Function (Segal, Stephenson, & Feldman, 2007) and determined that the baby was not a candidate for a frenulectomy. The baby did achieve a nutritive suck with intervention by the lactation consultant. For the previous 24-hour period, the neonate’s HR had been recorded in the 130s. A routine oxygen saturation value of 96% was obtained at 24 hours of life. At discharge, the infant was noted to have an HR of 87 beats per minute (bpm) with approximately seven to eight skipped beats; however, no murmurs were identified. Brachial and femoral pulses were equal and symmetrical. The infant was pink and appeared to be in no distress; the lung fields were clear to auscultation. He

exhibited normal reflex activity and good muscle tone. The HR rose to the upper 90s with gentle stimulation, and the skipped beats decreased. This finding was concerning and warranted additional evaluation, because 99% of newborns achieve an HR greater than 100 beats per minute (bpm; Dawson et al., 2009; Miller, Shannon, & Wetzel, 2000; Verklan, 2002). A full cardiac evaluation was initiated, and four extremity blood pressures revealed the following normal results: right arm, 58/31 mmHg; right calf, 75/51 mmHg; left arm, 66/37 mmHg; and left calf, 59/37 mmHg. A chest radiograph indicated normal cardiac contours, size, and normal bone structure, with no infiltrates of the lungs, pleural effusion, or pneumothorax. An electrocardiogram was obtained while the baby was in an alert state; a 2-minute rhythm strip indicated an HR of 105 bpm and normal sinus rhythm. The QT interval and the QRS were normal, indicating no heart block. A comprehensive review of the mother’s prenatal record was performed. Using a Spanish interpreter, the mother was questioned to ascertain that there was no previously unrecorded history of syphilis. The mother denied any complications in previous pregnancies and confirmed that her other children were

TABLE 2. Nurse’s assessment and routine medications Assessment/medication


Weight Length Frontal occipital circumference Ballard score for newborn maturation Vitamin K Penicillin G Erythromycin eye ointment Hepatitis B vaccine (Engerix-BÒ)

2670 g (20th percentile) 46 cm (20th percentile) 34.5 cm (70th percentile) 39-40 weeks 1 mg, intramuscular injection 60,000 Units, intramuscular injection ½-inch ribbon to each eye 10 mg, intramuscular injection

Note. Percentiles for weight, length, and frontal occipital circumference and the Ballard score for newborn maturation are from Thilo, E., & Rosenberg, A. (2012). The newborn infant. In W. Hay, M. Levin, R. Deterding, M. Abzug, & J. Sondheimer (Eds.), Current diagnosis and treatment: Pediatrics (21st ed.). New York NY: McGraw Hill Companies, Inc.


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healthy and that there was no family history of heart disease. She denied alcohol, tobacco, or drug use, including methadone. The intrapartum infant heart monitor strip was evaluated, revealing an HR of 110 to 120 with appropriate beat to beat variability during early labor and an HR of 120 to 160 during the second stage. Occasional decelerations to the 90s were noted during pushing, with brisk recovery between contractions. Meconium noted in the amniotic fluid raised suspicion for an anoxic event before birth and the risk of meconium aspiration and sepsis; however, the infant did not have respiratory difficulty, temperature instability, or feeding difficulty that would indicate an infectious process (Thilo & Rosenberg, 2012). Additionally, the neonate’s cord blood pH of 7.25 supported a lack of anoxia in utero (American Academy of Pediatrics [AAP] and American Heart Association [AHA], 2011). This well newborn appeared to have normal heart rate variation, and a diagnosis of transient neonatal bradycardia was made. Because the infant had no significant risks for sepsis and did not appear ill, blood cultures and a complete blood cell count were not obtained. Without a heart murmur and because of the presence of a normal electrocardiogram and chest radiograph, an echocardiogram was not indicated. A breastfeeding session was observed by a pediatric nurse practitioner (PNP) and a lactation consultant; no signs of gastroesophageal reflux were appreciated. A Spanish interpreter was used to explain the findings to the parents. As a precaution, the mother and infant were kept overnight for observation. The infant continued to room in with his mother, and vital signs and oxygen saturation rates were obtained every 4 hours. The on-call PNP checked on the dyad during the night shift to ascertain any concerns. Overnight, oxygen saturation values were 94% and 100%, and the HRs were between 100 and 135 bpm. The infant’s respiratory rate remained in the 40s. The infant had breastfed every 3 to 4 hours for 40- to 60-minute sessions. Prior to discharge, physical examination findings included an HR of 108 bpm with a regular rhythm, rising to 126 bpm while crying, and a respiratory rate of 42 breaths per minute. It appeared that the bradycardia had resolved. A follow-up appointment was made in a pediatric clinic for 3 days after discharge. The plan of care was reviewed with the parents, including signs and symptoms of cardiac failure and respiratory distress. They were assured that their baby had a normal examination and that the bradycardia appeared to be a result of the transition process to extrauterine life. If concerns were noted at the next appointment, the primary care physician would refer them to a pediatric cardiologist. Three days later, the infant arrived for the well-baby checkup. Breastfeeding continued to go well; he had gained weight and was now at his original birth weight. His HR was 120 to 140 bpm with a normal sinus rhythm.

Respirations were unlabored at 46 breaths per minute. The first newborn screen results were normal. The infant was examined at 2 and 4 months of life for routine newborn care. On physical examination the HR was 142 and 136 bpm, respectively, with a regular rhythm and no heart murmurs. At the 4-month visit, the infant had doubled his birth weight and was still receiving breast milk feedings. DISCUSSION A neonate undergoes several important changes at the time of birth that allow the transition to extrauterine life. During the delivery, the umbilical cord is clamped and the infant experiences changes to the pulmonary and cardiac systems that are in response to external stimulation of the new environment and internal physiologic changes. The fluid circulating in the fetal lungs is replaced by air (te Pas et al., 2009; Verklan, 2002). This process creates an increase in blood flow and pressure through the heart that facilitates the change from fetal to neonatal circulation. The heart undergoes increasing parasympathetic influences, resulting in a natural drop in rate over the first few minutes of life (Artman, Mahoney, & Teitel, 2010; Dawson et al., 2009). The HR may vary with changes in the newborn’s behavioral activity as a result of increasing vagal stimulation and subsequent competition of organs under parasympathetic control (Artman et al., 2010; Delco, Beghetti, & Pfister, 2009; Verklan, 2002). More than 90% of all infants make this transition without difficulty, and 99% are able to maintain an HR greater than 100 bpm, which has long been considered the most important clinical sign of an infant’s successful transition to extrauterine life (AAP & AHA, 2011; Dawson et al., 2009; Delco et al., 2009). An HR of less than 100 bpm is termed bradycardia. The management and prognosis of bradycardia depend on the underlying etiology (Miller et al., 2000). Heart rates between 80 bpm and 100 bpm are particularly confounding, because 99% of all infants achieve a rate of greater than 100 bpm; an HR less than 80 is usually considered pathologic (Dawson et al., 2009; Delco et al., 2009; Miller et al., 2000). The etiology of bradycardia can be divided into maternal and infant factors. Maternal autoimmune diseases, such as lupus, and infections, such as syphilis, can cause bradycardia in the fetus and newborn (Brucato, Previtali, Ramoni, & Ghidoni, 2010; Kakowaga et al., 2011). Maternal heart disease treated with beta blockers and severe preeclampsia may result in neonatal bradyarrhythmias (Heida, Zeeman, Van Veen, & Hulzebos, 2012; Ponnampalam, O’Brien, & Khalil, 2011). Methadone use during pregnancy may result in a prolonged QT interval and a slow HR in the neonate (Parikh, Hussain, Holder, Bhoyer, & Ewer, 2011). -/- 2014


Aspects of an infant’s anatomy and health may also contribute to the findings of bradycardia. Infant abnormalities, such as congenital heart disease with atrioventricular block or left bundle block, can result in neonatal bradycardia (Freire & Dubrow, 2008). Bradycardia may be a symptom of neonatal sepsis or intraventricular hemorrhage (Griffin, Lake, O’Shea, & Moorman, 2007). Anatomic respiratory obstruction, such as the rare incidence of esophageal hamartoma, may cause a slowing of the infant’s HR (Coury, Steinfeld, Zwillenberg, & Zwillenberg, 2010). Other causes of a slow HR include periods of apnea or gastroesophageal reflux, as seen in premature infants (Zhao, Gonzalez, & Mu, 2011). More commonly, episodic events of bradycardia are a result of the vagal response to infant activity and an immature nervous system (Dawson et al., 2009; Delco et al., 2009; Verklan, 2012). A review of fetal cardiac development and the transition to extrauterine life may help clarify the diagnosis of transient bradycardia in the newborn. The myocardium begins beating rhythmically by 3 weeks after conception. By 5 to 6 weeks, the HR can be detected by sonography, and the average rate is 110 bpm; at this time, the atrioventricular electromechanism controls the rate (Hornberger & Sahn, 2007). With further development of the conduction system, the HR increases to 170 bpm by the 10th week of gestation, and the sinoatrial node becomes the primary pacemaker of the cardiac contractions (Hornberger & Sahns, 2007). Parasympathetic control increases as the fetus develops and the rate begins to slow to 130 bpm by 40 weeks (Hornberger & Sahns, 2007). The fluid that fills the fetal lungs at birth must be removed to make room for air with the infant’s first breath (te Pas et al., 2009; Verklan, 2002). Uterine contractions during a vaginal delivery help with this process. Naturally occurring surfactant helps to reduce the surface tension of the lung tissue and open the alveoli in preparation for gas exchange (Verklan, 2002). The interruption of fetal circulation and the clamping of the cord cause a drop in the blood pH and a rise in partial pressure of carbon dioxide, which stimulates the first breath (Dawson et al., 2009; Verklan, 2002). The HR is difficult to obtain in the first minute of life. An oxygen saturation monitor is the most accurate assessment, but the device is hard to maneuver on the wet, slippery skin of the infant (Dawson et al., 2009). The average HR in a term infant greater than 37 weeks’ gestation in the first few minutes after birth is 110 to 180 bpm with a 5- to 15- beat variability (Dawson et al., 2009; Verklan, 2002). Dawson and colleagues (2009) studied a cohort of 468 term infants and found that only 1% had HRs less than 100 bpm at 5 minutes. They referred to this phenomenon as ‘‘reflex bradycardia’’ and attributed it to vagal stimuli or mild hypoxia during the birth process. The vagus nerve or the 10th cranial nerve stimulates 4

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the parasympathetic fibers of the heart, lungs, and gastrointestinal tract, as well as other organ systems (Artman et al., 2010). The normal process of birth, tactile stimulation, entering an environment that is colder than the uterus, and passing meconium stool can all result in confusion to an immature nervous system, which results in a vagal response and lowering of the newborn’s HR (Delco et al., 2009). Still, Dawson and colleagues (2009) found that the majority of newborns had an average HR of 142 to 171 bpm in the first few days of life and that 99% maintained an HR greater than 100 bpm. A healthy infant will have a 5- to 15-beat variability in response to different infant behaviors (Artman et al., 2010; Dawson et al., 2009; Delco et al., 2009). As the nervous system matures, coordination of the vagal feedback system improves and the HR is less influenced by changes in respirations, gastrointestinal stimulation, or other bursts of activity (Delco et al., 2009; Verklan, 2002). CONCLUSION Ninety-nine percent of infants maintain an HR greater than 100 bpm after the first few minutes of life. HR variability is often noted as a result of the differences in fetal and neonatal circulation and the increased role of the vagal innervation and parasympathetic control of the HR. This Most HRs less than variability is considered a healthy sign of 80 bpm are an infant’s transition to considered extrauterine life. Most pathologic, but a HRs less than 80 bpm are considered pathofew infants may logic, but a few infants exhibit episodes of may exhibit episodes rates in the 80s or of rates in the 80s or lower that are a result lower that are a of a hypervagal resresult of a ponse. As the sympahypervagal thetic system matures in the first few days of response. life, these bradycardia events resolve without intervention. Because some of the differential diagnoses can be devastating to a newborn, a thorough workup is warranted, and close observation is recommended. Keeping parents informed of the evaluation process and minimizing separation of the mother and infant is critical in assuring parents that their infant is most likely experiencing a normal transition to extrauterine life. REFERENCES American Academy of Pediatrics & American Heart Association. (2011). Neonatal resuscitation textbook (6th ed.). Washington, DC: American Academy of Pediatrics and American Heart Association.

Journal of Pediatric Health Care

Artman, M., Mahoney, L., & Teitel, D. (2010). Neonatal cardiology (2nd ed.). New York, NY: McGraw Hill Publishers. Brucato, A., Previtali, E., Ramoni, V., & Ghidoni, S. (2010). Arrhythmias presenting in neonatal lupus. Scandinavian Journal of Immunology, 72(3), 198-204. Coury, J., Steinfeld, J., Zwillenberg, D., & Zwillenberg, S. (2010). Esophageal hamartoma as an unusual cause of neonatal apnea and bradycardia. Ear, Nose and Throat Journal, 83(3), E7-E11. Dawson, J., Kamlin, C., Wong, C., te Pas, A., Vento, M., Cole, T., . Morley, C. (2009). Changes in heart rate in the first minutes after birth. Archives of Disease in Childhood, Fetal and Newborn Edition, 95, F177-F181. Delco, C., Beghetti, M., & Pfister, R. (2009). Vagal bradycardia at term. ACTA Paediatrica, 98, 901-909. Freire, G., & Dubrow, I. (2008). Accelerated idioventricular rhythm in newborns: A worrisome but benign entity with or without congenital heart disease. Pediatric Cardiology, 29, 457-462. Griffin, P., Lake, D., O’Shea, M., & Moorman, R. (2007). Heart rate characteristics and clinical signs in neonatal sepsis. Pediatric Research, 61(2), 222-227. Heida, K., Zeeman, G., Van Veen, T., & Hulzebos, C. (2012). Neonatal side effects of maternal labetalol treatment in severe preeclampsia. Early Human Development, 88(7), 503-507. Hornberger, L., & Sahn, D. (2007). Rhythm abnormalities of the fetus. Heart, 93, 1294-1300. Kakogawa, J., Sadatsuki, M., Masuya, N., Gomibuchi, H., Minoura, S., & Hoshimoto, K. (2011). Prolonged fetal bradycardia as the

presenting clinical sign in congenital syphilis complicated by necrotizing funisitis: A case report. ISRN Obstetrics and Gynecology, 2011, 320246, Retrieved from http://www.ncbi.nlm. Miller, M., Shannon, K., & Wetzel, G. (2000). Neonatal bradycardia. Progress in Pediatric Cardiology, 11(1), 19-24. Parikh, R., Hussain, T., Holder, G., Bhoyar, A., & Ewer, A. (2011). Maternal methadone therapy increases QTc interval in newborn infants. Archives of Disease in Childhood, Fetal and Newborn Edition, 96(2), F141-F143. Ponnampalam, S., O’Brien, P., & Khalil, A. (2011). Prescribing medications for heart disease in pregnancy. Prescriber, 19, 38-41. Segal, L., Stephenson, R., & Feldman, P. (2007). Prevalence, diagnosis, and treatment of ankyloglossia. Canadian Family Physician, 53(6), 1027-1033. te Pas, A., Arjan, B., Wong, C., Kamlin, C., Dawson, J., Morley, C., & Davis, P. (2009). Breathing patterns in preterm and term infants immediately after birth. Pediatric Research, 65(3), 352-356. Thilo, E., & Rosenberg, A. (2012). The newborn infant. In W. Hay, M. Levin, R. Deterring, M. Abzug & J. Sondheim (Eds.), Current diagnosis and treatment: Pediatrics (21st ed.). New York, NY: McGraw Hill Companies, Inc. Verklan, M. T. (2002). Physiologic variability during transition to extrauterine life. Critical Care Nursing Quarterly, 24(4), 41-56. Zhao, J., Gonzalez, F., & Mu, D. (2011). Apnea of prematurity: From cause to treatment. European Journal of Pediatrics, 170, 1097-1105.

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Bradycardia in a term newborn.

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