Reviewing Pediatric Arrhythmias
November 1, 2022 39 minutes read
Authors
Gesca H. Borchardt, MD, Resident of Pediatrics, Banner Children’s at Diamond Children's Medical Center, University of Arizona, Tucson
Katie Kowalek, MD, Assistant Professor of Pediatrics, University of Arizona, College of Medicine, Tucson
Peer Reviewer
Daniel Migliaccio, MD, Clinical Assistant Professor, Ultrasound Fellowship Director, Department of Emergency Medicine, University of North Carolina, Chapel Hill
Executive Summary
- Clues to malignant premature ventricular complexes (PVCs) include several QRS complexes of different morphologies on the electrocardiogram (ECG), a segment of three consecutive PVCs (classified as ventricular tachycardia), and PVCs that increase in frequency during exercise.
- Tachyarrhythmias are characterized by a heart rate (HR) above the upper limit of normal for age (> 95th percentile). The HR threshold is > 220 bpm in infants and > 180 bpm in children.
- Atrioventricular re-entry tachycardia and atrioventricular nodal re-entry tachycardia are the most common causes of supraventricular tachycardia (SVT) in a healthy child or adolescent, and in > 50% of cases, the first episode may occur < 1 year of age. A common treatment is adenosine, and in 17% of encounters for SVT, adenosine alone did not treat the tachyarrhythmia, and a second-line therapy was needed. Esmolol and amiodarone were the most common second-line therapy used, but in children younger than 1 year of age and in congenital heart disease, amiodarone was the preferred second-line agent.
- It is estimated that more than 300,000 children live with asymptomatic Wolff-Parkinson-White in the United States and that about 16% of SVTs are caused by WPW. Children’s risk of having sudden cardiac death (SCD) is more than double the risk of the adult population. The risk of a potential life-threatening event (LTE) in children with WPW is about 1% to 2% per year.
- In a structurally normal heart, bradycardias are more commonly caused by congenital heart block and sinus node dysfunction. Data are limited because of the rarity of these conditions in the pediatric population.
- In adults, athletes can tolerate HR > 30 bpm, but anything less than that rate should trigger a complete work-up. A study by Diaz-Gonzales et al evaluated more than 6,000 athletes between the ages of 5 and 16 years and determined that 99.9% of them had HR > 45 bpm. Therefore, it is acceptable to use 40 bpm as a threshold for initiating a work-up in this population.
- Congenital heart block is defined as heart block identified in utero and up to 27 days of life. It is lethal in 18% to 50% of fetuses and 2.5% to 15% in newborns. Most congenital heart blocks are caused by maternal autoimmune antibodies, with a predominance of complete atrial ventricular heart block (type 3) over types 1 and 2.
- First degree atrial-ventricular (AV) block may be considered benign in structurally normal hearts, but they increase the risk of malignant arrhythmias in congenital heart disease, infections (they have been observed in the early stages of SARS-CoV-2 in children, Lyme disease, and acute rheumatic fever), or medications (e.g., olanzapine, digitalis, and sodium- and calcium-channel blockers).
- Myocarditis, cardiomyopathy, or other tissue-damaging diseases need to be ruled out and treated, and, in cases with irreversible Mobitz type 2, implantable cardiac defibrillator (ICD) implantation is recommended because of the increased risk of evolution to complete AV block.
- Infections like Lyme disease, myocarditis, or Chagas disease also can cause complete AV block and must be ruled out. Close cardiac monitoring is recommended, and ICD is one of the treatments of choice because of the high risks of SCD.
- The main inherited cardiac arrhythmias are long QT syndrome, short QT syndrome, Brugada syndrome, and catecholamine polymorphic ventricular tachycardia. These are rare genetic electrical disorders of a structurally normal heart. Patients most commonly present with palpitations, dyspnea, and dizziness during physical activity or after an unexplained syncope episode, unexplained near drownings, or after a life-threatening arrhythmia episode (usually VF) and cardiac arrest. Initial diagnosis includes ECG and a detailed history, including current medications and a known history of an unexplained death of a young family member.
Although pediatric arrhythmias are uncommon, it is essential to recognize which ones require diagnostic evaluation and therapy and which ones do not. Frequently, there are normal variations on pediatric ECGs that do not require a significant evaluation, but recognizing critical arrhythmias in pediatric patients is a must-know for providers.
— Ann M. Dietrich, MD, FAAP, FACEP, Editor
Introduction
Although arrhythmias are less common in the pediatric population than in adults, it is important to know how to diagnose and treat them in children. It is estimated that 55.1 out of 100,000 pediatric patients visiting the emergency department (ED) are because of arrhythmias. There usually is a bimodal distribution between infants and adolescents.1 In a small study by Kharbanda et al, children with congenital heart disease already demonstrated atrial conduction abnormalities prior to corrective surgery and at a very young age (mean age 6 months).2 Dysrhythmias usually are classified based on pulse rate and need to be distinguished from normal variations.3
Tachyarrhythmias are classified as heart rates (HR) above the upper limit of normal and account for about 13.5% of pediatric ED visits for palpitations. Bradyarrhythmias are classified as HR below the lower limit of normal and absent pulse or cardiac arrest.1 Unlike in adults, the HR in the pediatric population changes with age. Therefore it is important to know the limits based on age. (See Table 1.) When providers suspect an arrhythmia, it is necessary to perform at 12-lead electrocardiogram (ECG), which increases the ability to detect any dysrhythmias that otherwise would be missed on a three-lead ECG.4
Table 1. Range for Pediatric Vital Signs5 |
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| Age Range | Heart Rate (Beats/Min) | Systolic Blood Pressure (mmHg) | Diastolic Blood Pressure (mmHg) | Mean Arterial Pressure (mmHg) | Respiratory Rate (Breaths/Min) |
Premature infant |
120-205 |
55-75 |
35-45 |
28-42* |
40-70 |
0-3 months |
110-160 |
60-85 |
30-55 |
45-60 |
30-60 |
3-6 months |
100-180 |
70-90 |
50-65 |
50-60 |
30-45 |
6-12 months |
90-130 |
80-100 |
55-65 |
50-62 |
25-40 |
1-3 years |
80-140 |
86-106 |
42-70 |
49-62 |
20-37 |
3-6 years |
70-120 |
89-112 |
40-75 |
58-69 |
20-28 |
6-12 years |
60-120 |
97-120 |
57-80 |
66-79 |
14-25 |
> 12 years |
60-100 |
100-131 |
64-83 |
73-84 |
12-20 |
*Mean arterial pressure approximates gestational age |
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Normal Variations
There are normal variations in pediatric ECGs that need to be recognized. When each of them appears in isolation, there is no need for a significant work-up, diminishing the child’s discomfort with multiple tests.
Sinus Arrhythmia
During respiration, the sinus rhythm can change abruptly and raise concerns for arrhythmia. The rhythm will increase with inspiration and then decrease with expiration — the pattern is reproducible. Unlike its name suggests, this is a benign variation. The action potential continues to originate from the sinus node, so the P wave’s morphology will not show drastic changes (unlike in ectopic atrial conduction). The P wave will be upright in leads aVF and I, with an axis between 0 and 90 degrees.3
Early Repolarization
Early repolarization presents as an ST elevation with a gradual upsloping of the segment in the leads where the T wave is positive.3
Benign rSR’
Lastly, in the V1 lead in adolescents, a normal QRS duration can have a secondary R’ wave, which is shorter than the original R wave.
Premature Beat
Usually asymptomatic and an incidental finding in ECGs, premature beats are mostly benign. If symptomatic, the patient will describe a single strong heartbeat or a “skipped” beat.3
Premature Atrial Complex
Premature atrial complex (PAC) represents most arrhythmias encountered in the neonatal period, but it can be seen in all ages. When discovered in isolation, PACs do not require further testing.6 These are contractions originating in the atrium and not generated by the sinus node, and the ECG will show an extra P wave. The morphology will be different than the sinus P wave. (Visit https://bit.ly/3ec66gU to see an ECG of a PAC.)
In structurally normal hearts, these contractions will conduct through the atrial-ventricular (AV) node if it is not in the repolarization phase of a sinus contraction, leading to ventricular contraction and extra QRS on ECG. The QRS will have the same morphology as the sinus rhythm QRS unless there is repolarization on the His bundle, which can broaden the QRS. Alcohol, tobacco, pregnancy, fatigue, coxsackievirus infections, digitalis toxicity, and structural heart disease can trigger PAC. Eliminating the triggers, if possible, will resolve the premature beat, and treatment with beta-blockers is recommended only in symptomatic patients.3,7,8
Premature Ventricular Complex
Premature ventricular complexes (PVCs) can be found in 40% of the pediatric population and are more common in teenagers and preteens.3,7,9 These are contractions that originate in the ventricle and that lead to an extra QRS on ECGs. The farther along the conduction pathway the origin of the contraction, the broader the QRS complex. If the origin is close to the bundle of His, the complex can be as narrow as the sinus QRS. These contractions are not preceded by a P wave, since they skip atrial contraction. (Visit https://bit.ly/3rBP7rk to see an ECG of a PVC.) They can be further classified as bigeminy (alternating sinus and abnormal QRS), trigeminy (two sinus QRS followed by an abnormal one), or couplet (two consecutive abnormal QRS).5 Although mostly benign when a single morphology is seen on the ECG, PVCs can be seen in myocarditis, channelopathies, and cardiomyopathy. Clues to malignant PVCs include several QRS complexes of different morphologies on the ECG, a segment of three consecutive PVCs (classified as ventricular tachycardia), and PVCs that increase in frequency during exercise. Benign PVCs are found in structurally normal hearts and tend to have a single QRS morphology, have decreased frequency with exercise, and be asymptomatic.
Triggers for PVCs include excessive caffeine consumption or levels of catecholamines, anxiety, electrolyte abnormalities (such as low potassium or magnesium and high calcium), stimulant-based medications (such as modafinil and methylphenidate) and illicit drugs (such as cocaine), alcohol, and tobacco.10,11 Other etiologies include sleep deprivation, hyperthyroidism, and structural cardiac abnormalities.12,13 Patients found to have PVCs not corrected by eliminating triggers should follow up with cardiology for Holter monitoring. If PVCs are found to be > 10% of the rhythm in the monitor, if there is ventricular dysfunction, or if the patient is symptomatic, continuous cardiology follow-up is recommended. Treatment includes anti-arrhythmia medications or foci ablation.3,7,9,14
Tachyarrhythmias
As previously described, tachyarrhythmias are characterized by an HR above the upper limit of normal for age (> 95th percentile). The HR threshold is > 220 bpm in infants and > 180 bpm in children.5 The presenting symptoms can vary from nonspecific feeding difficulties and fussiness to palpitations and chest pain. Prolonged arrhythmias can present with congestive heart failure (CHF), shock, or sudden death.15 There are many causes for tachycardia that include, but are not limited to, sepsis, hypovolemia, fever, anemia, drugs, and medications (beta agonists like albuterol, caffeine, and atropine). These conditions need to be addressed to resolve the tachycardia.5 The following sections will approach tachyarrhythmias by dividing them into narrow or broad QRS complexes (in adults < 120 ms vs. > 120 ms, respectively), with the understanding that pediatric QRS are age-dependent. Broad QRS in the pediatric population is defined as QRS > 98th percentile for the age.4, 15,16 (See Table 2.) This complex can be separated further into regular or irregular rhythm.1
Table 2. Pediatric Range for ECG Parameters5 |
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| Age Range | Heart Rate (Beats/Min) | PR Interval (Seconds) | QRS Duration (Seconds, 98th Percentile)* |
Premature infant |
120-205 |
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0-3 months |
110-160 |
0.08-0.12 |
0.05 (0.07) |
3-6 months |
100-180 |
0.08-0.13 |
0.05 (0.07) |
6-12 months |
90-130 |
0.10-0.14 |
0.05 (0.07) |
1-3 years |
80-140 |
0.10-0.14 |
0.06 (0.07) |
3-6 years |
70-120 |
0.11-0.15 |
0.07 (0.08) |
6-12 years |
60-120 |
0.12-0.17 |
0.07 (0.08-0.09)** |
> 12 years |
60-100 |
0.12-0.17 |
0.07 (0.10) |
*The 98th percentile for acceptable QRS interval **The 98th percentile is 0.08 for ages 6-8 years and 0.09 for ages 9-12 years. ECG: electrocardiogram |
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Narrow QRS Complex
Regular rhythm is defined as every atrial depolarization leading to a ventricular depolarization and every P wave followed by a QRS complex.5,17 The most common tachycardia is called supraventricular tachycardia (SVT), where it is difficult to determine if every QRS is preceded by a P wave. However, they all originate above the bundle of His and the ventricles. The heart will beat between 180-220 bpm in children and between 240-270 bpm in infants. On ECG, there will be fixed R-R interval.3,7,16-18 SVT includes:
- atrioventricular re-entry tachycardia (AVRT, re-entry is caused by the AV node and the presence of an accessory pathway, more common in infants);
- typical and atypical atrioventricular nodal re-entry tachycardia (AVNRT, re-entry caused by the AV node itself or AV node and foci at nearby atrial tissue, more common in adolescents);
- atrial tachycardia, which is not well differentiated on ECG.1,5,19,20
SVT affects one in 250-1,000 children and about one in 15 children with congenital heart disease.4,19,20 AVRT and AVNRT are the most common SVT in a healthy child or adolescent, and in > 50% of cases, the first episode may occur before the first year of life.18,21 AVRT will be present in 30% to 60% of children with ventricular preexcitation. It has a bimodal appearance with onset at 0-2 months of age and 63.4% reporting symptoms after the age of 5 years.18,20 In all, 93% of AVRT in infants younger than 2 months of age will disappear spontaneously, whereas 78% of AVRT with onset after 5 years of age will persist.18,22
Symptoms include presyncope, palpitations, and diaphoresis, but true syncope usually is not seen.3 In a study by Przybylski et al (2021), SVT was studied at 33 pediatric hospitals over a period of eight years. In their study, they found that 45.5% of patients had a history of a cardiac disease, congenital heart disease (CHD) was present in 27% of patients, and 26% of patients had ventricular preexcitation. Fifty-four percent of children had no preexisting or concurrent cardiac disease, and 20% of children were younger than 1 year of age.19 Thirty-five percent of children had readmission within the first 30 days of their initial visits.
Nonpharmacological ways to treat SVT in hemodynamically stable patients include stimulating the vagal response. Common vagal maneuvers include carotid massage, Valsalva movement, and ice to the face, and there is a case report of an infant whose Valsalva maneuver was caused by retching and emesis, successfully stopping SVT.3,21
The goal of treatment is the cessation of the tachyarrhythmia. A common treatment is adenosine, and in this study, the hospitalization rate for patients receiving adenosine as the treating agent was about 50%. In 17% of encounters for SVT, adenosine alone did not treat the tachyarrhythmia, and a second line therapies was needed. Esmolol and amiodarone were the most common second-line therapy used, but in children younger than 1 year of age and in CHD, amiodarone was the preferred second-line agent.18,19 In this sensitive age group, the provider needs to avoid verapamil and diltiazem because of the danger of provoking severe hypotension and cardiac arrest by decreasing cardiac output (these drugs cause negative chronotropic and inotropic effects on AV node and myocardium).4,15,19,23,24 In toxic doses, the selectivity of the calcium channel blocker decreases and results in decreased insulin release and increased vasodilation, amplifying cardiovascular compromise.25
As mentioned, SVT can be terminated with medications. Compared to older children, adenosine efficacy is lower in infants, at 9% to 35%. Adenosine is only recommended for hemodynamically stable children at the following doses:
- rapid bolus 0.1 mg/kg;
- can be increased up to 0.3 mg/kg4,19,26
However, adenosine can cause anxiety or a sense of impending doom. Therefore, it is important to prepare patients prior to drug administration.3 If adenosine fails, use amiodarone 5 mg/kg IV over 20 to 60 minutes or procainamide intraosseously/IV 15 mg/kg over 30 to 60 minutes.
- Amiodarone: load 5-10 mg/kg over 20 to 60 minutes, maintenance 5-15 mcg/kg/min;4,18,19,26
- Digoxin was used for prophylaxis of SVT in 8% of infants at a dosage to maintain a serum level of 0.6-1.3 nmol/L;4,6,18
- Flecainide (not available in the United States): 1.5-2 mg/kg over five minutes;
- Propafenone (not available in the United States): load 2 mg/kg over two hours, maintenance 4-7 mcg/kg/minutes;
In children older than 1 year of age, verapamil can be used at 0.1 mg/kg slowly over two minutes. Sotalol is another drug efficient in terminating AVRT with a safe profile:
- Loading dose 1 mg/kg injected within 10 minutes;
- Maintenance 4.5 mg/kg/day;
- Recommend in children with left ventricular ejection fraction (LVEF) > 50% and normal QTc.
Children older than 4 years of age/weighing at least 15 kg are eligible to receive catheter ablation.3,4,18 Untreated SVT can lead to tachycardiomyopathy; therefore, prompt response is recommended.
If a tachycardia episode lasts longer than 8.5 hours, cardiac dysfunction needs to be considered.22 In unstable patients, synchronized cardioversion starting at 0.5 J/kg to 1 J/kg is recommended.4,5,16 Side effects of the medications used for SVT treatment include QRS complex widening with sodium channel blockers (specifically propafenone) and hypotension with beta-blockers.18 When starting amiodarone, obtaining a baseline and monitoring of liver enzymes and thyroid function are recommended because of the risk of hepatotoxicity with transient increase in liver enzymes and because its iodine content and similarity to thyroid hormone can affect thyroid function.27,28
Previously, the evidence on the side effects of amiodarone in the pediatric population had been conflicting, but a recent study (THYRAMIO) found that close to 20% of children on amiodarone developed thyroid dysfunction (amiodarone-induced hypothyroidism or amiodarone-induced thyrotoxicosis), with the majority of those patients (55%) having congenital heart disease.27 Thyroid function is important to follow because of the negative neurocognitive effects of hypothyroidism.27,28
Atrial flutter is rare in children and is marked by regular atrial activity at 250-500 bpm. Newborns and children with CHD, especially after cardiac surgery, represent most pediatric cases.7,26 ECG will present the “sawtooth” pattern best seen in leads II, III, and aVF.7 Patients with accessory pathways may develop ventricular fibrillation from 1:1 ventricular conduction.26,29 Commonly mistaken with SVT, atrial flutter can be unmasked using adenosine. Adenosine briefly stops conduction through the AV node and will show tachycardia being conducted via an accessory pathway.26 The heart usually will beat from 250-350 bpm. Direct current cardioversion seems to be the most successful measure to stop atrial flutter.26,30
Irregular rhythm is described as atrial depolarization not always eliciting a ventricular depolarization. Atrial tachycardia has variable atrial rhythm while atrial fibrillation (AF) and multifocal atrial tachycardia are more irregularly irregular.5 Although atrial fibrillation is one of the most common sustained arrhythmias in adults, it is rare in the pediatric population, with an estimated prevalence of 0.001%, and it affects teenagers more often than younger children.30,31 The heart will beat at 350 bpm and up to 600 bpm, with a ventricular response ranging 110 bpm to 150 bpm with a regular QRS complex.5 If the patient has a structurally normal heart and function, the condition is called “lone” AF. However, it is seen more commonly in children with underlying cardiac conditions.7,31 As with SVT, if left untreated, AF can lead to tachycardiomyopathy and thromboembolism. If AF is associated with Wolff-Parkinson-White (WPW) syndrome, it can lead to ventricular fibrillation and death.29 Obesity and male gender were found to be risk factors for AF.30 On ECG, there will be low-voltage P waves with a variable and irregular R-R interval.7 Synchronized cardioversion seems to be the most successful measure to stop AF, and children with recurrent AF may benefit from cardiac ablation.26,30
Broad QRS Complex
Broad QRS complex tachycardias are more commonly ventricular in origin and consist of ventricular tachycardia (VT), with or without preceding P wave, and ventricular fibrillation (VF). Supraventricular tachycardias with bundle branch blocks, aberrancies, accessory pathways, or a delta wave can present with broad QRS complex. The differential also includes toxicity and electrolyte abnormalities.4 While SVT affects one in 250-1,000 children, VT affects one to eight in 100,000 children with HR at 120-150 bpm.4,9 There is a benign form of monomorphic VT called accelerated ventricular tachycardia (AVT), where the ventricles beat 15% to 25% faster than the expected sinus rhythm for age, or < 120 bpm in adolescents. In a structurally normal healthy heart without underlying disease, AVT can be treated like PVCs with longitudinal follow-up.3,9 Another benign VT is seen when the beat originates from the right ventricular outflow tract (RVOT). On the ECG, it will be seen as an inferior axis, wide-complex tachycardia with left bundle branch block (LBBB). This phenomenon will appear as positive QRS in the inferior leads (II, III, aVF). Ventricular beats originating in the left ventricle will have a right bundle branch block (RBBB) pattern.4,9 If the VT originates from one foci and is represented with regular QRS without P waves, it is called monomorphic and can present as ventricular flutter.4,7,12,29,30
Accessory pathways are connections from the atrium to the ventricles outside the common bundle of His. The most common atrio-ventricular accessory pathways are through the Kent bundle, which circles the left mitral annulus 25% of the time and circles the right tricuspid annulus 60% of the time. Fifteen percent are septal conductions. Septal accessory pathways have the highest risk of leading to a complete heart block after treatment with ablation.29 The right accessory pathway gives origin to a pathway connecting the bundle of His to the ventricle bypassing the AV node and causing ventricular preexcitation. On ECG, this phenomenon is seen as a delta wave with shortening of the PR interval and widening of the QRS complex17,22
Anterograde conduction through the accessory pathway is described as WPW, while retrograde conduction is termed permanent junction reciprocating tachycardia (PJRT). AF can occur in hearts with accessory pathways. When the conduction is anterograde, such as in WPW, irregularly irregular wide QRS beats are seen (called preexcitation atrial fibrillation).4,32 It is estimated that more than 300,000 children live with asymptomatic WPW in the United States and that about 16% of SVTs are caused by WPW.15,29 Children’s risk of having sudden cardiac death (SCD) is more than double the risk of the adult population. The risk of a potential life-threatening event (LTE) in children with WPW is about 1% to 2% per year, but clear LTEs occur in only 0.1% to 0.5% of children. A potential LTE is AF, whereas a clear LTE is VF and SCD.22,29 A more benign symptom is SVT, which can lead to AF and the more lethal VF.29,31 (Visit https://bit.ly/3fH1DmJ to see an ECG of WPW.)
Some forms of VT and VF have irregular rhythms and account for about 10% of all cardiopulmonary resuscitation (CPR) events.33 As mentioned, some SVTs in the setting of AV conduction delay (from a block) can present with broad QRS complex. Because VT has higher mortality than SVT, it is safer to assume and treat the rhythm as VT and not SVT.4,7,9,16
Polymorphic VTs arise from multiple foci. They are rare in children, and their presences require a thorough examination.3 A commonly known polymorphic VT is torsades de pointes, which could indicate polypharmacy with medications that commonly prolong the QT interval or underlying long QT syndrome.4,7,17,34,35 (See Table 3.) VF is a disordered ventricular arrhythmia in which the heart no longer beats effectively, and it is estimated to account for 8% of SCD cases.7,32,36 It is estimated that one out of 10 survivors of idiopathic ventricular fibrillation are younger than 16 years of age.37 Cardiomyopathies and channelopathies are the most common causes of VF in the pediatric population.4,37
Table 3. Common Drugs Used in the Pediatric Population Known to Cause QTc Prolongation38-47 |
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| Antimicrobials/Antifungals | Antipsychotics/Antidepressants | Gastrointestinal-Affecting Drugs | Antiarrhythmics | Others |
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This is not a comprehensive list. Please use resources in the reference for more information |
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More commonly, immediate treatment will be to follow the Pediatric Advanced Life Support (PALS) algorithm, especially in unstable patients.4,33,36 The defibrillator should be attached promptly. For pulseless VT or VF, the shock will start with 2 J/kg. If a pulse is present, synchronized cardioversion can be started at 0.5-1 J/kg for atrial flutter and fibrillation, SVT, or stable ventricular tachycardia.4,5,16 There is an estimated 7% to 10% increase in mortality with each minute of delay for defibrillation in adults, but this association was not found in children, most likely because the majority of pediatric cardiac arrest happens in the intensive care unit (ICU).33
Following the algorithm, the shock can have progressively increasing power, up to a maximum of 10 J/kg. Epinephrine is the first-line medication to administer at a dosing of 0.01 mg/kg every three to five minutes, and its delay can be detrimental to the outcome in children.33 Amiodarone 5 mg/kg or lidocaine 1 mg/kg can then be administered for patients who remain unstable.4
Stable patients should have a good personal and family history taken to identify reversible causes of VT (medications, electrolyte abnormalities, congenital heart disease, inherited arrhythmias, toxin ingestions, etc.).4,36 Remembering that VT can be caused by SVTs, adenosine and vagal maneuvers may be attempted in stable patients.4 About 57% of patients may experience recurrence of ventricular arrhythmias, reinforcing implantable cardiac defibrillator (ICD) as the mainstream treatment for these arrhythmias.36 Pharmacological maintenance therapy should only be started with close monitoring by pediatric cardiology, and a more in-depth review of pharmacological treatment for chronic ventricular tachycardia is beyond the scope of this review.4
Bradyarrhythmias
As previously described, bradycardia is defined as a heart rate below the lower limit of normal.5 (See Table 1.) In a structurally normal heart, bradycardias are more commonly caused by congenital heart block and sinus node dysfunction. Data are limited because of the rarity of these conditions in the pediatric population. Bradycardia can be normal in pediatric athletes, but data on the appropriate range are lacking. In adults, athletes can tolerate HR > 30 bpm, but anything less than that rate should trigger a complete work-up.
A study by Diaz-Gonzales et al evaluated more than 6,000 athletes between the ages of 5 and 16 years and determined that 99.9% of them had HR > 45 bpm. Therefore, it is acceptable to use 40 bpm as a threshold for initiating a work-up in this population.5,48 Other causes of bradycardia include nicotine, hypoxia, electrolyte abnormalities (e.g., hyperkalemia, hypercalcemia), vagal stimulation, increased intracranial pressure, hypothyroidism, and hypothermia. Common medications that can lead to bradycardia include opioids, beta-blockers, cholinesterase inhibitors such as physostigmine, and digoxin.5,49,50 Cholinergic toxins, such as organophosphates, and cholinergic toxidrome mimics (pesticides, such as amitraz, and herbicides, such as chlorophenoxy compounds) are known to cause bradycardia as part of their toxidrome.51-53
Patients will present with nonspecific symptoms, such as syncope, easy fatigue, and concern for seizures. Night terrors also have been associated with nocturnal bradycardia in certain cases.54 Extrinsic causes of bradycardia with poor perfusion in the pediatric population usually are in the setting of respiratory insufficiency or shock and are a sign of impending cardiac collapse.33,55,56 It is estimated that 15,000 children will receive in-hospital CPR annually in the United States, with about a 50% survival rate. Outside of the hospital, the survival rate decreases significantly because it depends on bystander CPR. More than 50% of CPR provided in the hospital is due to bradycardia.33,56
In a study by Khera et al, about 30% of children with bradycardia and poor perfusion progressed to pulselessness in the hospital setting.55 Given the severity of this symptom, PALS recommends CPR to be initiated if HR < 60 bpm to deter development into cardiac arrest.55 In this study, 59% of pediatric patients with bradycardia were already on mechanical ventilation. A survival rate of 70% was achieved in bradycardia patients when they were treated before pulseless events occurred and, thus, were not allowed to progress to pulselessness. The survival decreased to < 40% if the event progressed to pulselessness, and the outcome worsened the longer the period between CPR initiation and the development of a pulseless rhythm.33,55,56
Congenital Heart Block
Congenital heart block is defined as heart block identified in utero and up to 27 days of life. It is lethal in 18% to 50% of fetuses and 2.5% to 15% in newborns.54,57,58 Most congenital heart blocks are caused by maternal autoimmune antibodies, with a predominance of complete atrial ventricular heart block (type 3) over types 1 and 2.3,54,58,59 It is estimated that between 2% and 5% of infants from mothers with autoimmune disease (specifically anti-Ro and anti-La) and who do not yet have affected children will have congenital complete heart block, with an incidence of one in 25,000 children. The incidence increases to 12.5% to 25% if a prior child has congenital heart block.6,54 During prenatal testing, bradycardia will be noted on cardiac M-mode tracings, and structural defects can be evaluated in fetal echocardiograms. These abnormalities could lead to premature delivery.54,57 The AV block can lead to congestive heart failure in newborns, and an epicardial pacing system (EPS) is recommended for any newborn with HR pauses of > 3 seconds, CHF, wide QRS, or QT prolongation.57
Prolongation of the PR interval manifests after atrio-ventricular block and can be divided into three categories.17 Type 1 (first-degree AV block) is seen as fixed prolonged PR interval (> 98% for age) on ECG, and this prolongation can be subtle.3,17,25,59,60 (See Table 2 and visit https://bit.ly/3fMGMyD to see an ECG of a first-degree AV block.) They can be considered benign in structurally normal hearts, but they increase the risk of malignant arrhythmias in congenital heart disease, infections (they have been observed in the early stages of SARS-CoV-2 in children, Lyme disease, and acute rheumatic fever), or medications (e.g., olanzapine, digitalis, and sodium- and calcium-channel blockers).5,61 They are associated with increased vagal reaction and usually improve with exercise (increase in sympathetic stimulation). If they are being caused by infections or medications, treatment for symptomatic patients includes addressing the causing agent. Otherwise, no treatment is required if it is an isolated ECG change. 3,62-65
Type 2 (second-degree AV block) occurs with partial and intermittent AV blocks. There are two main subtypes — Mobitz type 1 (commonly called Wenckebach) and Mobitz type 2. There are other, less common subtypes as well. Mobitz type 1 and type 2 usually present with lightheadedness, syncope, and palpitation and can be incidental findings. They include ECG findings, such as every other P wave generating a QRS (called a 2:1 AV block), or two or more P waves in a row to generate a single QRS (called a high-grade AV block). Mobitz type 2, 2:1 AV block, and high-grade AV block all warrant further evaluation for abnormalities below the AV node.3
In Mobitz type 1 (Wenckebach), the PR intervals increase with each beat until there is a failed AV conduction, called QRS drop. (Visit https://bit.ly/3SHUbqa to see an ECG of a Mobitz type 1.) The beat will pick up on the next contraction. This pattern is benign, and, like type 1 AV block, Wenckebach also is associated with vagal reaction and usually is an incidental finding. It can be appreciated in sleeping younger individuals during a state of high vagal tonicity or in awake athletes.3
In Mobitz type 2, the P wave will intermittently not conduct through the AV node, causing dropped QRS without PR prolongation. (Visit https://bit.ly/3CdAHTk to see an ECG of a Mobitz type 2.) This always is pathological because it indicates an issue after the AV node and is rare in the pediatric population. Myocarditis, cardiomyopathy, or other tissue-damaging diseases need to be ruled out and treated, and, in cases with irreversible Mobitz type 2, ICD implantation is recommended because of the increased risk of evolution to complete AV block.3,17,59
Complete AV block presents as dissociation between the P wave and the QRS complex, meaning the P wave will not generate a QRS complex. (Visit https://bit.ly/3V8HPJ5 to see an ECG of a third-degree AV block.) Symptoms are variable depending on the rate of the “escape rhythm” and causing agent. The escape rhythm indicates where the signal for ventricular depolarization is originating, such as junctional or ventricular rhythm. The rate and symptoms also depend on the presence of other arrhythmias or structural abnormity. This type of AV block will show up with symptoms related to syncope or palpitations. However, in more severe cases, the patient may present with cardiac failure or SCD. Infections like Lyme disease, myocarditis, or Chagas disease also can cause complete AV block and must be ruled out. Close cardiac monitoring is recommended, and ICD is one of the treatments of choice because of the high risks of SCD.3,17,59
Inherited Sinus Node Dysfunction
The sinus node, located on the right atrium by the superior vena cava, generates action potential that is considered the pacemaker of the heart.7,32 In case of dysfunction, it causes P waves that are inappropriately slow, leading to bradycardia and pauses longer than three seconds on ECG. They are commonly seen in the elderly population and can be caused by procedures involving the atria, infective diseases, and stress. These are uncommon in children, but they can be caused by muscular dystrophy, channelopathies, and some inherited forms of arrhythmias.7,17,32 A permanent pacemaker/ICD is recommended to all children with irreversible bradycardia.54,57
Inherited Arrhythmias and Channelopathies
Inherited arrhythmias and channelopathies account for about 10% to 20% of sudden death in the pediatric population.57,66 The main inherited cardiac arrhythmias are long QT syndrome (LQTS), short QT syndrome (SQTS), Brugada syndrome (BrS), and catecholamine polymorphic ventricular tachycardia (CPVT). These are rare genetic electrical disorders of a structurally normal heart. Patients most commonly present with palpitations, dyspnea, and dizziness during physical activity or after an unexplained syncope episode, unexplained near drownings, or after a life-threatening arrhythmia episode (usually VF) and cardiac arrest.32,37,57,67,68 Initial diagnosis includes ECG and a detailed history, including current medications and a known history of an unexplained death of a young family member.
Long QT Syndrome
LQTS is the most common inherited channelopathy and is suspected to account for 10% to 15% of suspected sudden infant death syndromes (SIDS) cases.57 The QT interval is measured from the beginning of the QRS complex to the end of the T wave, with better measurements in leads II and V5, and prolongation is defined as an interval of > 450 ms in prepubertal girls and > 440 ms in prepubertal boys. (Visit https://bit.ly/3MaPCSG to see ECG features of long QT syndrome.) The QT interval needs to be corrected by the Bazett formula to account for variations caused by heart rate. Any corrected QT of > 500 ms is pathological and needs further work-up.3,17,38,57,66,68
It is estimated that one in 2,000 healthy live-born children will have LQTS. 34,68 Three mutation genes account for 75% to 90% of cases, whereas 15% to 20% of patients remain genotypically negative.34,57,68 Most patients present in the first 20 years of life with syncope, cardiac arrest, or SCD. Syncope is the strongest predictor for SCD, increasing the likelihood of LTEs 10- to 20-fold.68 Because this is a genetic condition, testing is recommended on all first-degree family relatives. Holter monitoring and exercise stress testing are recommended as part of the work-up. When exercising, there will be a paradoxical prolongation of the QTc interval with an increase in heart rate. The prolongation is caused by delayed ventricular repolarization, putting cardiomyocytes at risk for early afterdepolarization during phases two and three of action potential. If the cardiomyocytes are synchronous, this triggers ventricular tachycardia, but if the potential is rapid enough, it can result in re-entrant ventricular excitation, leading to torsade de pointes.4,17,34,35
On ECG, there will be a distinct prolongation of the QT interval in leads II and V5.34 The ECG may also show changes on the T wave, such as T-wave inversions on V1-V3.69 Arrhythmia’s risk increases when ECG shows a QTc interval > 500 ms and T-wave alternans.57,66,68-70
Pharmacological treatment is with noncardioselective beta-blockers. Propranolol and nadolol are effective, whereas metoprolol and atenolol have uncertain efficacy.3,34,57 Even then, beta-blockers only have better efficacy on LQT1 mutations.68 Postpartum patients are at an increased risk of experiencing life-threatening arrhythmias. Therefore, beta-blockers should be prioritized in the first nine months postpartum. In patients with LQT3 gene mutation, mexiletine, a sodium channel blocker, shortens the QTc interval and can improve management.57,68 Nonpharmacological treatment involves left cardiac sympathetic denervation and implantation of an ICD, which is recommended in more severe cases (syncope on beta-blockers, QT > 550 ms, and survivors of LTEs).57,68 It is important to stress that family members need to learn CPR. If the child is very young, an automatic external defibrillator can be used, and the child can switch to an ICD later. Triggers for arrhythmic events include QT-prolonging drugs, dehydration, hypokalemia, and hyperthermia. There are three main genes to be aware of, since having one of these genes indicates specific known triggers:35,57,68
- LQT1: Recommend limiting exposure to physical and emotional stress. Activities to be aware of are swimming and diving.57,68
- LQT2: Recommend avoiding sudden noises when sleeping (e.g., alarms and cell phones) because auditory stimulation and sudden arousal may lead to dysrhythmia. Also, this group of people should avoid hypokalemia.57,68
- LQT3 has night arrhythmia events, commonly VF and torsades de pointes. Recommendations include adding an intercom or other forms of easy communication to the room in case the patient feels the sudden onset of symptoms and needs help quickly and efficiently.57,68
- Both LQT2 and LQT3 cause events that are not silent, and adults should recognize gasping sounds and seek help. Families should know how to perform CPR and have a defibrillator close by.57
Individuals susceptible to QT prolongation may show normal ECG unless a stressor is present. Moreover, several drugs prolong QT and must be monitored closely in these individuals.35
Short QT Syndrome
SQTS is a rare autosomal dominant syndrome with a high mortality rate because of its significant rate of ventricular arrhythmias.17,35 There is a male predominance, and it affects about 0.05% of the pediatric population. Most patients will have cardiac arrest between the ages 14 and 20 years. Patients usually have a strong family history of a young first- or second-degree family member with a history of syncope or SCD.
ECG monitoring of newborns is recommended in patients with a strong family history. Minor symptoms include palpitations, syncope, atrial fibrillation, and atrial flutter. Gain of function mutation on potassium channels causes shortened repolarization of the action potential. On ECG, a shortened QT interval will be present (< 330-340 ms) with an absent or minimal ST segment.57,71,72 T waves may appear peaked, similar to those seen in hyperkalemia. The J point to T peak interval usually is < 120 ms.71 ICD is the recommended treatment, but, because quinidine induces QT prolongation, it can be administered. Sotalol, which also prolongs QT, was found to be ineffective on the most common genetic mutation found in SQTS.
Brugada Syndrome
BrS is extremely rare in children, with an estimated prevalence of < 0.01%. However, it is responsible for an estimated 4% to 12% of SCD.57 It affects males disproportionally (8:1).68 Unlike the other inherited arrhythmias, BrS syncopal episodes occur at rest during the night, when vagal stimulation is decreased. It can be induced by fevers, including after vaccinations.32,67 Given this pattern, it is recommended to perform a complete 12-lead ECG in any febrile child with a family history suspicious for BrS or SCD. The 12-lead ECG also is recommended in all children with febrile seizures, since the fever unmasks BrS.67,68 It is suggested that using higher precordial leads on the third intercostal space (ICS) vs. the regular fourth ICS can help diagnose BrS on ECG. ECG is diagnostic for type 1 disease and will show high J point with coved-type ST elevation (> 2 mm) in V1-V3 and a negative T wave. (Visit https://bit.ly/3EmGacZ to see the ECG features of BrS.) Conduction delay is shown as prolonged PR and QRS intervals, usually with a right bundle block pattern. The findings are intermittent, and sodium channel blockers (e.g., flecainide, procainamide, and the more specific ajmaline) can help unmask the ECG features.32,35-37,67,68,72 In a study by Conte et al, 23% of children who survived sudden cardiac arrest without identifiable causes had ECG changes associated with BrS when a repeat test with sodium channel blockers was performed after puberty.37, 73 Types 2 and 3 cannot be diagnosed solely on ECG and need to show conversion to a type 1 on ECG with the administration of a sodium channel blocker. ECG for types 2 and 3 show the “saddleback” ST segment appearance, with type 2 having a greater elevation than type 3.68
About 20% of children with BrS may have SVT and AF, which can lead to ventricular arrhythmias. Life-threatening events in children with BrS are estimated to be around 10%. A point award system created by Gonzales-Corcia and collaborators can calculate the risk of potential lethal events based on symptomology and ECG findings. Any person with more than four points is recommended to receive an ICD, while anyone with six points or greater has a 53% risk for LTEs.67,68
Catecholaminergic Polymorphic Ventricular Tachycardia
CPVT is mostly an autosomal dominant condition, although there have been reports of recessive genes. Children usually present between 3 to 16 years of age, and many are misdiagnosed with epilepsy because the observed syncope episodes can have rhythmic movements.68 It is estimated that CPVT accounts for 10% to 15% of SIDS cases and 35% of SCD cases without structural abnormalities.57 More commonly, the mutation causes a calcium leak from the sarcoplasmic reticulum during diastole.57,68,69 With increases in heart rate, such as during exercise/activity or stress to above 110-130 bpm, the risk of VF increases because of the premature ventricular beat.35,68 Patients will present with palpitations and exercise-/stress-induced near syncope, seizure, or SCD. Bidirectional ventricular beats are pathognomonic of CPVT, which presents similarly to digitalis toxicity.4,57,68,69
Recommended pharmacological treatment, similar to that for LQTS, is with long-acting beta-blockers, such as nadolol and carvedilol, at the highest dosing tolerated. For example:
- Nadolol (preferred): 1-2 mg/kg/day;
- Metoprolol: 1-3 mg/kg/day;
- Propranolol: 3-4 mg/kg/day68
About 30% of patients still will manifest VF even when on medication.57 Adjunction of flecainide improves efficacy, and an ICD is recommended only to patients surviving LTEs because the shock administered by the ICD itself can trigger an LTE.35 Amiodarone, magnesium, and lidocaine have been useful in patients with ICD discharge to decrease further and recurrent discharges.57
Arrhythmias and COVID
More recently, SARS-CoV-2 has taken over the world, and it has been shown to spread easily among the population. It is estimated that, in the first year of the pandemic, 2% to 5% of SARS-CoV-2 cases were in children.74,75 Upon exposure, 40% of children < 18 years of age develop symptoms. In people > 18 years of age, the rate rises to about 80%. Only 20% to 30% of children exposed to the virus will become symptomatic.75 It is known that patients with preexisting cardiovascular disease tend to have a poorer prognosis with COVID-19 infection.35 Children with CHD post-surgical correction seem to be at a significantly increased risk for cardiac manifestations.70,74
Malignant arrhythmias caused by the infection have not been well documented, but they have been noted in the literature. In children, SVT, first-degree AV block, and RBBB are seen more commonly.70 The literature has been diverse regarding the involvement of the cardiovascular system and its connection to arrhythmias. A review by Sperotto et al reported that arrhythmias were found in 7% to 60% of children with multisystem inflammatory syndrome in children (MIS-C), while some multicenter studies in Europe found ECG abnormalities in 27% to 35.3% of patients admitted to the hospital with MIS-C and cardiac symptoms.70,74,76,77
The most common ECG abnormalities were nonspecific, but they included changes in ST segment in 22% of cases, prolonged PR interval in 6.3% to 16% of cases, QTc prolongation in about 3% to 22% of cases, transient AV block in about 25% of cases, and premature ventricular depolarization in 1% of cases.60,61,74,76-78 A study by Regan et al indicated that up to 67% of children will show ECG abnormalities, and about 50% of them will have T-wave inversion.60,74 There have been reports of late-onset bradycardia in the setting of myocarditis associated with MIS-C. First-line treatment should be IV immunoglobulin and glucocorticoids, and second-line treatment should use anakinra.79,80 In adults, a study has shown that arrhythmias were present in 17% of non-ICU patients and up to 44% of ICU patients. With the inherited arrhythmias, depending on the genetic defect present, it is possible that COVID-19 causes pro-arrhythmic effects, given its signs and symptoms of fever, stress, and electrolyte disturbances, and the more widespread use of antiviral drugs.35,70
It is imperative to provide close monitoring with ECG and a more aggressive approach to fever to avoid these effects in susceptible individuals. Several drugs provided during infection care can impair ventricular repolarization, prolonging the QT interval and potentially leading to malignant arrhythmias.35,70,74 Moreover, many drugs inhibit CYP3A4, increasing the effect of QT-prolonging drugs. Drugs that have been used previously for the treatment of SARS-CoV-2 and inhibit CYP3A4 include chloroquine and hydroxychloroquine, azithromycin, and remdesivir. As per the most recent COVID-19 Treatment Guidelines published by the National Institutes of Health (NIH), chloroquine, hydroxychloroquine, and azithromycin are not recommended for the treatment of SARS-CoV-2 infection. The newest recommendations include the use of ritonavir-boosted nirmatrelvir as the primary treatment choice, followed by remdesivir as a secondary choice. In case reports, remdesivir has been shown to cause sinus bradycardia, and this symptom improved with the discontinuation of the drug.81-83 Ritonavir is a strong CYP3A4 inhibitor and is used to increase the blood concentration of nirmatrelvir — consequentially strongly interacting with many other medications. The list of drug-drug interactions can be found in the NIH COVID-19 Treatment Guidelines and is beyond the scope of this review.84,85 The combination of any of these drugs and any other QT-prolonging drugs needs to be closely monitored in patients with LQTS. Care also must be taken to avoid hypokalemia and to ensure high serum potassium, since it is a known trigger in LQTS.35,74
Fevers can be potentially malignant in patients with BrS because it is one of the triggers for LTEs and unmasking ECG findings. In children with BrS, fevers were associated with 6% of LTEs. However, in children younger than 5 years of age, fever is associated with close to 65% of LTEs. Children with BrS and fevers of > 38.5°C despite antipyretic treatment need to be evaluated promptly in the ED and be observed until type 1 ECG findings are no longer appreciated.35,74
Patients with SQTS may benefit from the QT-prolonging drugs used during SARS-CoV-2 and do not seem to be at higher risk of malignant arrhythmias during the infection. 35,74
Fever has not been shown to trigger LTEs in patients with CPVT, but patients who are very sick and need hemodynamic support might be at increased risk. Epinephrine can unmask VF and be damaging during cardiac arrest in the CPVT population.35,74 Cardiac medications in patients with genetic arrhythmias and channelopathies should be continued in the setting of COVID-19 infection.74 It is important to note that the ECG abnormalities resolved in the European studies, and 93% to 97% of children with SARS-CoV-2 infection had favorable outcomes and were discharged home.60,74,77
Conclusion
Although less common than in adults, dysrhythmias in pediatric patients can be harder to diagnose and present with nonspecific symptoms. Given these characteristics, it is important to recognize their specific ECG findings and know the appropriate treatment. A visit to the ED during LTEs usually is the first time a dysrhythmia will be identified. Therefore, mastery of these conditions and their treatment is imperative. In this review, the most common tachyarrhythmias, bradyarrhythmias, inherited channelopathies, and normal variations were summarized. Additionally, their definitions, epidemiologies, risk factors, diagnoses, and treatments based on the most current literature were included. Finally, the ranges for pediatric vitals and ECG findings were covered.
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Although pediatric arrhythmias are uncommon, it is essential to recognize which ones require diagnostic evaluation and therapy and which ones do not. Frequently, there are normal variations on pediatric ECGs that do not require a significant evaluation, but recognizing critical arrhythmias in pediatric patients is a must-know for providers.
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