A two-day-old male infant, born at 30 weeks’ gestation, develops sustained tachycardia with heart rates ranging from 180 to 220 beats per minute. He is hemodynamically stable with normal urine output. A sepsis evaluation is performed, and a radiograph shows the tip of his umbilical venous catheter located in a normal position at the inferior cavoatrial junction. An electrocardiogram (EKG) is obtained while adenosine (indicated by the green arrow) is administered for diagnostic purposes (Figure 1).1
Figure 1. Electrocardiogram (EKG) of the patient in the vignette with adenosine administration (green arrow), with specific findings in V4 noted in black, yellow, and blue arrows. Image adapted from: Carney M, Kalhan T, Rochelson E. Tachycardia in a premature neonate. Neoreviews. (2024);25(1):e56–e59.1
Which of the following is the most accurate description of the EKG findings shown in Figure 1?
- Irregular rhythm, narrow QRS complex, and ectopic P waves
- Irregular rhythm, wide QRS complex, and atrioventricular (AV) electrical dissociation
- Regular rhythm, narrow QRS complex, absent P waves, and AV electrical discordance
- Regular rhythm, wide QRS complex, retrograde P waves, and AV dissociation
- Regular rhythm, narrow QRS complex, absent P waves, and ventricular preexcitation
Answer: D. Regular rhythm, wide QRS complex, retrograde P waves, and AV dissociation
Explanation:
The patient in the vignette is hemodynamically stable with persistent tachycardia and an EKG demonstrating a regular rhythm with wide QRS complex, retrograde P waves (Figure 1, black arrows), and AV electrical dissociation (Figure 1, blue arrows). These findings are most consistent with ventricular tachycardia (VT).1,2 VT is an abnormal rhythm originating from the ventricular myocardium or Purkinje cells below the Bundle of His.1,2 It is defined as three or more consecutive premature ventricular complexes (PVC) with AV dissociation.3 VT in neonates is most commonly idiopathic but can be seen in patients with cardiac tumors, myocarditis, and electrolyte abnormalities.1 Monomorphic VT presents with an uniform QRS shape, a regular rhythm and a wide QRS complex due to uncoordinated or slow ventricular depolarization.1–6 If polymorphic, VT can present with an irregular rhythm and beat-to-beat variability in QRS shape.6
Electrocardiographic features of VT include a wide QRS complex and AV dissociation (Figure 1) (Option D). This AV dissociation can be demonstrated with three pathognomonic features:
- P waves running slower than the ventricle, which causes notched QRS complexes.
- Presence of “capture beats,” which are isolated normal QRS complexes in between VT rhythms that occur as a result of a normal sino-atrial node impulse.
- Presence of “fusion beats,” which are isolated dysmorphic QRS complexes that occur as a result of the ventricle being depolarized by a normal sino-atrial node impulse and the VT arrhythmia at the same time.1,4,5
The management of VT depends upon clinical stability, as assessed by blood pressure, capillary refill, muscle tone, and level of consciousness.1 If the infant remains hemodynamically stable, first-line medications include intravenous (IV) lidocaine, IV esmolol, or oral propranolol.1,2,4 If hemodynamically unstable (hypotonia, decreased responsiveness, hypotensive, and increased capillary refill), defibrillation must be performed.1,3,4 An important differential diagnosis for VT is supraventricular tachycardia (SVT) with aberrancy. Adenosine can aid in differentiating between rhythms. When adenosine is given during VT, a loss of retrograde P waves (Figure 1, yellow arrows) will occur without interruption in the tachycardia. However, in patients with SVT with aberrancy, adenosine can terminate the tachycardia resulting in conversion to sinus rhythm and visualization of the P wave prior to the QRS complex.1,4,5
Atrial flutter (AF) presents as a narrow QRS complex tachycardia, caused by an ectopic focus in the right atrium. Patients with AF can have “sawtooth flutter” waves on the EKG, and atrial rates may be as high as 300 beats/min.2,7 The rhythm is often irregular, because the AV conduction is variable (Figure 2) (Option A).2,5,7 Structural heart disease and malpositioned central venous catheters are common causes of AF.2 The presence of this rhythm in utero can be associated with structural cardiac anomalies and may progress to fetal hydrops. Medications such as digoxin or propranolol can be used in the management of AF.2,7 Although the patient in the vignette has an umbilical venous catheter, the radiograph demonstrates appropriate catheter tip position, and the presence of a wide-complex tachycardia, regular rhythm, and absence of the classic sawtooth pattern on EKG makes AF less likely.
Figure 2. Patient with atrial flutter demonstrating classic “sawtooth waves” pattern (blue arrows) and variable block, causing an irregular rhythm. Image adapted from: Pike JI, Greene EA. Fetal and neonatal supraventricular tachyarrhythmias. Neoreviews. 2012;13(10):e605-614.7
In neonates with an irregularly irregular rhythm and a wide QRS complex, Torsades de pointes (“twisting of peaks”) should be suspected (Figure 3) (Option B).2,6,8 Torsades, a form of polymorphic VT, can be seen with electrolyte derangements (hypokalemia and hypomagnesemia) and congenital long QT syndrome.2,6,8 Congenital long QT syndrome may initially be associated with bradycardia, but it ultimately increases the patient’s risk of having ventricular fibrillation and sudden cardiac death.2,6,8 First-line pharmacotherapy for Torsades is IV magnesium, followed by defibrillation, per the current Pediatric Advanced Life Support (PALS) algorithm.6,8 The patient in this vignette is hemodynamically stable and presents with a wide-complex monomorphic tachycardia. These features are inconsistent with the polymorphic EKG features of torsades de pointes.
Figure 3. EKG of a patient with CHD who is noted to have initially a narrow complex tachycardia, which terminates briefly, followed by a normal QRS complex that leads into a wide complex tachycardia consistent with Torsades de Pointes (“twisting of peaks”) (blue arrows), as noted with an irregular rhythm with complete AV dissociation. Image adapted from: Panchangam C, Vachharajani A. An abnormal echocardiogram and telemetry tracing in a late preterm infant. Neoreviews. 2021;22(11):e790-794.8
Junctional ectopic tachycardia (JET) is a narrow QRS complex tachycardia most frequently seen in the post-operative period following cardiac surgery and/or cardiopulmonary bypass, with a focus arising distal to the AV node in the Bundle of His.2,9 Cardiac surgeries, including arterial switch operation, AV canal repair, the Norwood procedure, Tetralogy of Fallot repair, and ventricular septal defect repair have been associated with JET.9 The congenital form is rare and is associated with significant mortality.2,3 EKG findings in JET include a narrow QRS complex, absent P waves, and AV discordance (Figure 4) (Option C) with an atrial rate slower than the ventricular rate (P wave-to-QRS complex ratio ≤ 1).2,4 Management options may include hypothermia, sedation, reduction of catecholamine-releasing medications (eg, epinephrine), and in select cases, antiarrhythmics (eg, amiodarone, procainamide).9 The patient in this vignette presents with wide QRS complexes on EKG and is less likely to have JET given the lack of cardiac surgery history or alternative means of disruption in conduction distal to the AV node.
Figure 4. Patient with congenital junctional ectopic tachycardia (JET) with atrioventricular (AV) discordance as noted by non-conducted P waves (black arrows) and narrow QRS complexes (blue arrows). Image adapted from: Baskar S, Czosek RJ. Evaluation and management of common neonatal arrhythmias. Neoreviews. 2020;21(9):e605-615.2
Tachycardias caused by an accessory pathway result in AV reentrant tachycardia (AVRT), where the accessory pathway can be both antegrade (i.e., atrium to ventricle) or retrograde (ie, ventricle to atrium).2,7,10 In orthodromic AVRT, the tachycardia circuit occurs down the AV node and up the accessory pathway.2,10 When antegrade, AVRT presents on EKG as a retrograde P wave followed by a QRS complex, a narrow QRS complex, and a delta wave denoting ventricular preexcitation (Figure 5) (Option E).2,7,10 These features can be seen in Wolf-Parkinson-White Syndrome.2–4 Adenosine is the drug of choice for blocking the AV node and terminating the tachycardia seen in AVRT.2–4 Due to the wide QRS complexes seen on the EKG in this vignette, this patient is less likely to have SVT due to AVRT.
Figure 5. Narrow QRS complex tachycardia with a P wave closely following the QRS complex (black arrows) and the presence of delta waves (blue arrows). These findings can be seen in orthodromic AV reentrant tachycardia or AV nodal reentrant tachycardia. Image adapted from: Baskar S, Czosek RJ. Evaluation and management of common neonatal arrhythmias. Neoreviews. 2020;21(9): e605-615.2
Did you know?
- The most commonly diagnosed fetal tachyarrhythmia is reentrant SVT due to an accessory electrical pathway.7
- Fetal bradycardia due to AV conduction disease is most commonly secondary to a complete heart block. Approximately 50% of fetal complete heart block cases have detectable autoantibodies in the respective pregnant person (anti-SSA/Ro and/or anti-SSB/La) and typically manifests at 16–18 weeks of gestation.11
What medications are used in the management of SVT in neonates?
For a detailed step-by-step algorithm for the management of SVT, refer to Figure 8 in Singh HR, Garekar S, Epstein ML, L’Ecuyer T. Neonatal supraventricular tachycardia (SVT). Neoreviews. 2005;6(7):e339-350.10
NeoQuest January 2024 Authors
Srirupa Hari Gopal, MBBS, FAAP, Baylor College of Medicine
Faith Kim, MD, Columbia University Medical Center
References:
- Carney M, Kalhan T, Rochelson E. Tachycardia in a premature neonate. Neoreviews (2024) 25 (1): e56–e59
- Baskar S, Czosek RJ. Evaluation and management of common neonatal arrhythmias. Neoreviews. 2020;21(9):e605-615
- Ban JE. Neonatal arrhythmias: diagnosis, treatment, and clinical outcome. Korean J Pediatr. 2017;60(11):344
- Kothari DS, Skinner JR. Neonatal tachycardias: an update. Arch Dis Child Fetal Neonatal Ed. 2006;91(2):F136
- Katritsis DG, Brugada J. Differential diagnosis of wide QRS tachycardias. Arrhythm Electrophysiol Rev. 2020;9(3):155-160
- Gupta R, Gelt V, Gow R. Case 2: Wide-complex tachycardia in a newborn. Neoreviews. 2016;17(8):e481-483
- Pike JI, Greene EA. Fetal and neonatal supraventricular tachyarrhythmias. Neoreviews. 2012;13(10):e605-614
- Panchangam C, Vachharajani A. An abnormal echocardiogram and telemetry tracing in a late preterm infant. Neoreviews. 2021;22(11):e790-794
- Sasikumar N, Kumar RK, Balaji S. Diagnosis and management of junctional ectopic tachycardia in children. Annals of Pediatric Cardiology. 2021;14(3):372
- Singh HR, Garekar S, Epstein ML, L’Ecuyer T. Neonatal supraventricular tachycardia (SVT). Neoreviews. 2005;6(7):e339-350
- Killen SA, Fish FA. Fetal and neonatal arrhythmias. Neoreviews. 2008;9(6):e242-252