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Management and evaluation of wide QRS complex tachycardia in children

Management and evaluation of wide QRS complex tachycardia in children
Literature review current through: Jan 2024.
This topic last updated: Sep 23, 2022.

INTRODUCTION — Wide QRS tachycardia may be due to ventricular tachycardia (VT), supraventricular tachycardia (SVT) with aberrant conduction, or atrioventricular (AV) reentrant tachycardia with an accessory pathway. Children with wide QRS complex tachycardia may present with hemodynamic instability, and, if not emergently treated, serious morbidity or death may occur. (See "Pediatric advanced life support (PALS)".)

The management and evaluation of wide QRS complex tachycardia in children will be presented here. The causes of wide QRS complex tachycardia in children are discussed separately. (See "Causes of wide QRS complex tachycardia in children".)

DEFINITIONS — The following terms are used throughout this topic:

Tachycardia – Tachycardia in children is generally defined as a heart rate above the normal range for age (ie, >160 beats per minute for infants under age two, >140 beats per minute for children 2 to 12 years old, and >100 beats per minute for adolescents and adults (table 1)).

Wide QRS complex – Wide QRS complex is defined by a QRS duration >80 milliseconds in younger children and >100 milliseconds in adolescents.

INITIAL MANAGEMENT — Assessment of the patient's hemodynamic status takes precedence over any diagnostic evaluation.

Cardiac arrest — Any patient who is unresponsive or pulseless is in cardiac arrest, and cardiopulmonary resuscitation should be initiated immediately, according to the pediatric cardiac arrest algorithm (algorithm 1) developed by the American Heart Association (AHA) and the International Liaison Committee on Resuscitation (ILCOR) [1]. (See "Pediatric advanced life support (PALS)", section on 'Pulseless arrest algorithm'.)

Once the patient is stabilized, further evaluation should be performed to identify the underlying cause of tachycardia and determine whether corrective therapy is indicated. (See 'Initial evaluation' below and 'Ventricular tachycardia' below.)

Unstable patient — Patients who are conscious and have palpable pulses but who have evidence of poor perfusion require prompt assessment and intervention. Such patients are at risk for cardiac arrest, especially if the underlying arrhythmia is ventricular tachycardia (VT) or preexcited atrial fibrillation.

Initial treatment — For initial treatment of patients with wide QRS complex tachycardia who are unstable (those who have palpable pulses but with poor perfusion), we recommend the following (algorithm 2) [2] (see "Pediatric advanced life support (PALS)", section on 'Tachycardia algorithm'):

Assess the airway and circulatory system. Provide airway management, oxygenation, and ventilation as needed. (See "Technique of emergency endotracheal intubation in children" and "Assessment of systemic perfusion in children".)

Attach an electrocardiogram (ECG) monitor or defibrillator with a rhythm display. The QRS duration for the patient is determined from the ECG rhythm. If time allows, a 12-lead ECG should be obtained for later review as this can help establish the diagnosis and guide therapy.

If the QRS is >80 milliseconds in infants and children or >100 milliseconds in adolescents (wide QRS complex tachycardia), the origin of the arrhythmia is assumed to be ventricular.

Synchronized cardioversion (0.5 joules to 1 joule per kg) is recommended to convert the arrhythmia to normal sinus rhythm. In conscious patients, sedation is suggested for the cardioversion if it does not delay procedure.

If the initial shock is not effective, a second cardioversion with an increased dose (2 joule per kg) is administered.

These recommendations are consistent with the 2010 AHA/ILCOR consensus international resuscitation guidelines [2]. In the 2015 and 2018 AHA/ILCOR updates, the algorithm for pediatric cardiac arrest was revised but the guidelines for tachyarrhythmias remained unchanged [1].

Shock-resistant tachyarrhythmia — If the second cardioversion is ineffective and the rhythm is not consistent with torsades de pointes (waveform 1A-B), antiarrhythmic therapy can be used before a third cardioversion attempt. Treatment of torsades de pointes is discussed below. (See 'Torsades de pointes' below.)

Options for initial antiarrhythmic therapy include lidocaine, procainamide, and amiodarone. The 2018 AHA/ILCOR recommendations state that either lidocaine or amiodarone may be used for shock-refractory VT [1]. Lidocaine is our preferred first-line antiarrhythmic in this setting, largely because it has a more favorable side effect profile. However, all of these drugs have potential for serious adverse effects and, therefore, consultation with a pediatric cardiologist is advised.

First-line – We suggest lidocaine as the first-line antiarrhythmic agent for acute management of children with wide complex tachyarrhythmia. We prefer lidocaine over procainamide and amiodarone because it has a more favorable side effect profile; it appears to have (based on limited clinical evidence) equivalent, if not superior, efficacy; and there is greater experience with this agent in children. Another advantage of lidocaine over amiodarone and procainamide is its reported efficacy in the treatment of arrhythmias associated with the channelopathies or as a consequence of QT prolonging agents [3-6].

Lidocaine is given with an initial bolus dose of 1 mg/kg intravenously (IV), and this may be followed by an infusion of 20 to 50 mcg/kg per minute. The bolus dose can be repeated if the infusion is initiated >15 minutes after the initial bolus dose. In an observational study of children with pulseless VT, lidocaine was associated with greater likelihood of return of spontaneous circulation and survival at 24 hours compared with amiodarone; however, neither drug was associated with increased likelihood of survival to discharge [7]. Severe adverse events related to IV lidocaine are uncommon; toxicity can include cardiovascular depression, drowsiness, disorientation, muscle twitching, and seizures. Serum levels should be monitored in patients requiring continuous therapy for >24 hours, in patients with signs of neurologic side effects (eg, seizures), or when large resuscitation doses are administered. Toxicity may occur with levels >6 mcg/mL. (See "Primary drugs in pediatric resuscitation", section on 'Lidocaine'.)

Second-line – Second-line antiarrhythmic agents include amiodarone, procainamide, and sotalol:

AmiodaroneAmiodarone is given slowly (over 20 to 60 minutes) at a dose of 5 mg/kg (maximum dose 300 mg) IV. Additional doses can be given in patients who remain in VT and do not have signs of toxicity (eg, hypotension, prolonged QT interval). Adverse effects are common and can be severe, including hypotension, bradycardia, atrioventricular (AV) block, vomiting, and nausea [8-10]. ECG and blood pressure monitoring should be performed during administration of amiodarone. (See "Primary drugs in pediatric resuscitation", section on 'Amiodarone'.)

Amiodarone use in infants and children can cause cardiovascular collapse with acidosis and ventricular dysfunction [11]. Amiodarone causes hypotension due to an intrinsic vasorelaxant effect and secondary to histamine release from the formulation that contains the solvent polysorbate 80. Additionally, amiodarone causes calcium channel blockade, which is poorly tolerated in infants. IV amiodarone has been subjected to randomized and blinded testing in children. In this trial, dose-related adverse events were common, including hypotension (36 percent), bradycardia (20 percent), and AV block (15 percent). In the highest-dose group of 10 mg/kg, hypotension was reported in 45 percent of subjects [10].

ProcainamideProcainamide is administered as a 15 mg/kg bolus IV over 30 to 60 minutes. There are limited clinical data regarding the use of procainamide in infants and children [2,12]. Procainamide tends to lengthen repolarization, which may be problematic in children with arrhythmia due to a channelopathy or QT prolonging agent.

ECG and blood pressure monitoring are required when procainamide is given. Because both amiodarone and procainamide can prolong the QT interval, they should not be administered together unless care is supervised by a clinician with expertise in treating children with arrhythmias. (See "Primary drugs in pediatric resuscitation", section on 'Procainamide'.)

Sotalol – IV sotalol is an additional antiarrhythmic option for acute arrhythmia termination. Data on use of sotalol in children with VT are limited. In single-center studies, it appears to be well tolerated with a low rate of adverse events, no deaths, and no malignant arrhythmias reported [13]. In a study of acute termination in pediatric patients, 30 mg/m2 given IV over 15 minutes converted most patients [14].

Torsades de pointes — If the rhythm is consistent with torsades de pointes (waveform 1A-B), IV magnesium sulfate at a dose of 25 to 50 mg/kg (maximum dose 2000 mg) should be given. Lidocaine may also be effective for treatment of torsades de pointes. (See "Primary drugs in pediatric resuscitation", section on 'Magnesium sulfate' and "Primary drugs in pediatric resuscitation", section on 'Lidocaine' and "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management".)

Further evaluation and management — Once the patient is stabilized, further evaluation should be performed to identify the underlying cause of tachycardia and determine whether corrective therapy is indicated. (See 'Initial evaluation' below and 'Ventricular tachycardia' below.)

Stable patient — In a patient who is hemodynamically stable, additional time can be given to determine whether wide QRS complex tachycardia is due to VT or supraventricular tachycardia (SVT) with aberrant conduction. Differentiation between the mechanisms guides further management choices in terminating the arrhythmia. Consultation with a pediatric cardiologist is advised. (See 'Evaluation for underlying cardiac disease' below and "Causes of wide QRS complex tachycardia in children".)

Goals — In a stable patient with wide QRS complex tachycardia, the goals of the initial evaluation include the following:

Determine if the wide QRS complex tachycardia originates from the ventricles or is supraventricular with aberrant conduction. The treatment and long-term prognosis differ between children with VT and those with SVT. (See 'Electrocardiography' below.)

Determine what therapeutic intervention(s) is required acutely or may be helpful in determining the underlying cause.

In addition, the initial evaluation will provide clues to aid in making a specific diagnosis and determine the need for further testing and/or corrective intervention. (See 'Ventricular tachycardia' below and "Management of supraventricular tachycardia (SVT) in children".)

Initial evaluation — The evaluation includes history, physical examination, ECG, and laboratory tests (including serum electrolytes and, when appropriate, antiarrhythmic drug levels).

Ongoing monitoring — Children with wide QRS complex tachycardia can quickly decompensate and become hemodynamically unstable even if they initially appear stable with adequate perfusion. Resuscitation equipment (eg, oxygen, defibrillator) should be made readily available, and, if the patient is in an outpatient setting, he/she should be transported to an emergency department by emergency medical services. This is especially true if there is underlying structural or functional heart disease.

Patients should have ongoing monitoring for signs of impending respiratory failure or compensated shock for as long as the wide QRS complex tachycardia persists. This includes continuous ECG monitoring, continuous respiratory and pulse oximetry monitoring, frequent blood pressure measurements (every 5 to 15 minutes), and frequent reassessment of the child's physical examination. Concerning findings include the following:

Hypotension

Hypoxia

Signs of respiratory distress (eg, tachypnea, nasal flaring, retractions, grunting) or signs of inadequate respiratory effort (eg, decreased respiratory rate, effort, or excursion)

Cool extremities, prolonged capillary refill, or weak peripheral pulses compared with central pulses

If any of these signs of compromised perfusion develop, synchronized cardioversion (0.5 joules to 1 joule per kg) should be performed, as described above. (See 'Initial treatment' above.)

History — The history is directed towards identifying patients with cardiac conditions (such as congenital long QT syndrome, acquired QT prolongation, arrhythmogenic cardiomyopathy, catecholaminergic VT, or Brugada syndrome) that are associated with VT. These patients are at risk for sudden cardiac death and require further evaluation and therapeutic interventions. (See "Causes of wide QRS complex tachycardia in children" and "Congenital long QT syndrome: Epidemiology and clinical manifestations" and "Acquired long QT syndrome: Definitions, pathophysiology, and causes" and "Brugada syndrome: Clinical presentation, diagnosis, and evaluation".)

History of heart disease – A child with congenital heart disease (CHD), especially one who has undergone cardiac surgery, is at increased risk for VT and sudden cardiac death.

Family history – A family history of sudden cardiac death, drowning, or sudden infant death syndrome may be elicited in patients with inherited cardiac disorders associated with VT. These include congenital long QT syndrome, Brugada syndrome, short QT syndrome, arrhythmogenic cardiomyopathy, catecholaminergic polymorphic VT (CPVT), or hypertrophic cardiomyopathy. (See "Congenital long QT syndrome: Epidemiology and clinical manifestations", section on 'Clinical manifestations' and "Congenital long QT syndrome: Epidemiology and clinical manifestations", section on 'Sudden infant death syndrome' and "Causes of wide QRS complex tachycardia in children".)

Medications – Many medications are associated with acquired QT prolongation and VT, including antiarrhythmic drugs (quinidine or procainamide), some nonsedating antihistamines (terfenadine or astemizole), macrolide antibiotics, certain opioids (eg, methadone), and antipsychotic and antidepressant medications (table 2). In addition, antiarrhythmic drugs can cause aberrancy during SVT, resulting in wide QRS complex tachycardia. (See "Acquired long QT syndrome: Definitions, pathophysiology, and causes" and "Cardiac excitability, mechanisms of arrhythmia, and action of antiarrhythmic drugs".)

Diseases causing metabolic derangements – Patients who develop hypokalemia or hypomagnesemia are at increased risk for acquired QT prolongation and VT (table 2). These conditions may be due to excessive urinary losses of these elements from drugs or renal tubular disorders, or inadequate dietary intake. Patients with anorexia nervosa also have prolonged QT intervals, which may cause arrhythmias and sudden death. (See "Acquired long QT syndrome: Definitions, pathophysiology, and causes" and "Anorexia nervosa in adults and adolescents: Medical complications and their management", section on 'Cardiovascular'.)

Cardiac symptoms – Symptoms are important in assessing the severity of hemodynamic compromise and may provide clues as to the specific underlying diagnosis. Symptoms related to tachyarrhythmia include palpitations, lightheadedness, weakness, diaphoresis, chest discomfort or pain, or syncope. In infants and nonverbal young children, parents may report nonspecific symptoms of poor feeding, irritability, and loss of consciousness. Hypoxic seizures may be secondary to syncope.

A history of a previous episode of syncope or seizures and the activity at the time of the episode are important. Events during sleep versus those during activity can be related to the underlying VT diagnosis. Fever-related episodes of VT or syncope should raise the suspicion for Brugada syndrome or long QT syndrome. (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation".)

Symptoms may be related to ventricular dysfunction due to associated heart disease (such as hypertrophic or dilated cardiomyopathy or myocarditis) rather than to the elevated heart rate. (See "Clinical manifestations and diagnosis of myocarditis in children", section on 'Clinical manifestations' and "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation".)

Physical examination — In addition to assessing the hemodynamic status of the patient (see 'Ongoing monitoring' above), the physical examination focuses on detecting signs of cardiac dysfunction or disease (eg, cardiac failure or structural heart disease) that may provide clues to the underlying cause of tachycardia:

Respiratory – Increased respiratory rate and effort.

Liver – Hepatomegaly.

Cardiac – Gallop and/or murmur.

Peripheral edema (rare in infants).

Dysmorphic features suggesting a syndrome that can be associated with ventricular arrhythmias, such as Barth syndrome (and noncompaction cardiomyopathy), Timothy syndrome (long QT type 8), and Andersen-Tawil syndrome (long QT type 7). (See "Inherited syndromes associated with cardiac disease", section on 'Barth syndrome' and "Genetics of dilated cardiomyopathy", section on 'Barth's syndrome' and "Causes of wide QRS complex tachycardia in children", section on 'Channelopathy' and "Congenital long QT syndrome: Pathophysiology and genetics".)

Electrocardiography — In a patient with wide QRS complex tachycardia, an ECG is helpful in differentiating between VT and SVT and determining the underlying VT diagnosis. However, definitive diagnosis is not always possible and may be time-consuming, especially for clinicians unfamiliar with the criteria for distinguishing VT from SVT. Consultation with a pediatric cardiologist is always warranted in the evaluation and management of stable patients with wide QRS complex tachycardia.

If there are any questions regarding the patient's stability, detailed ECG evaluation should be deferred in favor of urgent therapy. If time allows, an ECG should be obtained for later review because this can help establish the diagnosis and guide therapy. (See 'Unstable patient' above.)

To perform an adequate ECG analysis, both a 12-lead ECG and a rhythm strip should be obtained. If available, a previous ECG when the patient was in normal sinus rhythm is useful.

ECG features that are useful in distinguishing VT from SVT include:

AV dissociation – AV dissociation (atrial activity that is independent of ventricular activity) is usually best detected in an inferior lead where the P wave is most prominent and the QRS complex is the most modest. AV dissociation generally establishes VT as the underlying mechanism of the wide QRS complex tachycardia, although AV dissociation can occur in junctional ectopic tachycardia.

In AV dissociation, dissociated P waves are recorded at a rate slower than the ventricular rate (waveform 2). Capture beats (dissociated P wave activates the ventricle prior to the next VT complex) and fusion beats (simultaneous activation of the ventricle by the dissociated P wave and the ventricle) may be seen in AV dissociation (waveform 3). However, in some cases of VT, there is no AV dissociation, because of retrograde conduction from the ventricle to the atrium. (See "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'AV dissociation'.)

Axis – Right superior axis (-90 to ±180) or an axis shift of more than 40° than the axis observed in normal sinus rhythm suggests VT.

QRS duration – Wider QRS complex is more suggestive of VT. In adults, a QRS duration >160 milliseconds is a strong predictor of VT. However, in infants and small children, the QRS duration may be much narrower, especially left ventricular (LV) fascicular VT.

Concordance – Concordance is present when the QRS complexes in all six precordial leads (V1 through V6) are monophasic with the same polarity. They can either all be entirely positive with tall, monophasic R waves or all be entirely negative with deep monophasic QS complexes. If any of the six leads has a biphasic QRS (qR or RS complexes), concordance is not present. Concordance (either positive or negative) strongly suggests VT; however, its absence is not helpful diagnostically. (See "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'Concordance'.)

The evaluation of ECG in wide QRS complex tachycardia is discussed in detail separately. (See "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'Evaluation of the electrocardiogram'.)

Laboratory tests — Serum potassium and magnesium should be measured as part of the initial evaluation because both hypokalemia and hypomagnesemia can prolong QT interval resulting in VT. (See "Acquired long QT syndrome: Definitions, pathophysiology, and causes", section on 'Metabolic abnormalities'.)

In patients with underlying heart disease who are taking digoxin, quinidine, flecainide, or procainamide, plasma concentrations should be measured to determine whether drug toxicity is a causative factor for tachyarrhythmia.

Management

Empiric intervention — An empiric IV dose of adenosine (0.1 mg/kg, maximum initial dose 6 mg) may be given by rapid bolus in stable patients with a wide QRS tachycardia if SVT with aberrant conduction is suspected based on the criteria outlined above. (See 'Electrocardiography' above and "Primary drugs in pediatric resuscitation", section on 'Adenosine'.)

The response to adenosine can be useful in distinguishing SVT from VT [15]. Adenosine is effective in treating many types of SVT and some forms of VT (ie, right ventricular outflow tract [RVOT] tachycardia and idiopathic left VT [ILVT]) [16]. Consultation with a pediatric cardiologist is advised in making the determination of the type of tachycardia and deciding whether to empirically treat with adenosine. (See "Management of supraventricular tachycardia (SVT) in children" and "Causes of wide QRS complex tachycardia in children", section on 'Right ventricular outflow tract tachycardia' and "Causes of wide QRS complex tachycardia in children", section on 'Idiopathic left ventricular tachycardia'.)

Specific therapy — After determining the origin of the wide QRS complex tachycardia in the stable patient, treatment can be targeted to the specific arrhythmia.

Ventricular tachycardia — In stable patients with VT, antiarrhythmic therapy is tailored according to the most likely underlying diagnosis. This should involve consultation with a pediatric cardiologist or electrophysiologist to assist in reviewing the ECG data and determining the likely underlying VT diagnosis.

Options for initial antiarrhythmic therapy include the same agents as are used in unstable patients (ie, lidocaine, amiodarone, and procainamide) [1,2]. However, certain types of stable monomorphic VT (eg, outflow tract VT and idiopathic LV VT) may respond to less aggressive antiarrhythmic medications, such as calcium channel blockers or beta blockers. Case reports of cardiovascular collapse with the use of IV amiodarone should caution against its routine use, particularly outside of the intensive care unit and without pediatric cardiology/electrophysiology consultation [11]. Synchronized cardioversion under moderate sedation is another option for terminating VT in stable patients and may be safer if there is a concern about cardiac dysfunction or long QT syndrome or acquired QT prolongation. Most but not all VT will respond to cardioversion. (See 'Shock-resistant tachyarrhythmia' above.)

Considerations based upon the specific VT diagnosis are as follows:

ILVT – ILVT (also called intrafascicular verapamil-sensitive reentrant tachycardia or Belhassen tachycardia) has a right bundle branch block morphology with a left superior frontal plane axis and a relatively narrow QRS duration (typically 0.12 to 0.14 sec) (waveform 4). It is often confused with SVT because of its ECG morphology. ILVT can be treated with calcium channel blockers (eg, verapamil) and occasionally responds to adenosine. Vagal maneuvers, beta blockers, and lidocaine are generally ineffective. (See "Causes of wide QRS complex tachycardia in children", section on 'Idiopathic left ventricular tachycardia' and "Ventricular tachycardia in the absence of apparent structural heart disease", section on 'Idiopathic left ventricular tachycardia'.)

Outflow tract tachycardia – The right and left ventricular outflow tracts (RVOT and LVOT) are both common sites of origin of VT in patients without structural heart disease, and the underlying mechanism is likely triggered activity. VT originating from the RVOT is more common than from the LVOT.

RVOT tachycardia is a benign condition that may resolve spontaneously. It is thought to be a cAMP-mediated triggered activity, and, as such, it is responsive to termination with vagal maneuvers, adenosine, calcium channel blockers, and beta blockers. A major challenge for the clinician is to distinguish children with RVOT tachycardia from the more serious arrhythmogenic RV cardiomyopathy (ARVC), which has a high risk of sudden cardiac death. An incidental presentation and slow VT generally are more characteristic of patients with RVOT tachycardia compared with those with ARVC. The VT associated with ARVC is usually due to reentry and does not respond to vagal maneuvers or adenosine. It is more likely to require cardioversion or pace-termination. The distinction between RVOT tachycardia and ARVC is important as the natural history and chronic therapies are substantially different. (See "Causes of wide QRS complex tachycardia in children", section on 'Right ventricular outflow tract tachycardia' and "Arrhythmogenic right ventricular cardiomyopathy: Anatomy, histology, and clinical manifestations".)

CPVT – In patients with CPVT (which is a bidirectional VT thought to be the result of triggered activity (waveform 5)), VT may be less responsive to electrical cardioversion until it degenerates into ventricular fibrillation. In these patients, there may be multiple episodes of VT and even electrical storm. Discontinuation of inotropic agents and treatment with the beta blocker esmolol may result in resolution of the VT. Oral beta blockers and flecainide are proven effective in the chronic management of VT in patients with CPVT [17]. Symptomatic patients may benefit from a left cardiac sympathetic denervation. (See "Catecholaminergic polymorphic ventricular tachycardia".)

Acquired QT prolongation – The cornerstone of the management of patients with acquired QT prolongation is addressing the underlying cause by identifying and stopping any precipitating drug as well as aggressive correction of any metabolic abnormalities, such as hypokalemia or hypomagnesemia. IV magnesium sulfate is first-line therapy for both the treatment and prevention of recurrence of long QT-related ventricular ectopy or torsades de pointes. (See "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management".)

Patients without an apparent VT diagnosis – For patients without an apparent VT diagnosis, when pharmacologic intervention is felt to be necessary, we suggest lidocaine rather than amiodarone or procainamide as the initial antiarrhythmic agent. The rationale for our preference for this agent in stable patients is the same as in unstable patients (ie, it has a more favorable side effect profile; it has equivalent, if not superior, efficacy; and there is greater experience with lidocaine in children). Sotalol is a relatively new agent for the treatment of VT and appears safe and effective in small single-center studies [13,14]. Synchronized cardioversion under sedation is another option for terminating VT in stable patients and may be safer if there is a concern about cardiac dysfunction or long QT syndrome or acquired QT prolongation. Most but not all VT will respond to cardioversion. (See 'Shock-resistant tachyarrhythmia' above.)

Supraventricular tachycardia — Stable patients with SVT and aberrant conduction resulting in wide QRS complex tachycardia are managed in the same manner as other patients with SVT.

The management of SVT is summarized in the table (table 3) and discussed in detail separately. (See "Management of supraventricular tachycardia (SVT) in children", section on 'Acute management'.)

CHRONIC MANAGEMENT

Ventricular tachycardia — After the acute episode of ventricular tachycardia (VT) is terminated, the clinician must decide whether further evaluation and/or corrective therapy such as ablation or the placement of an implantable cardioverter-defibrillator (ICD) are indicated. These decisions need to be made by a clinician with expertise in pediatric electrophysiology.

Key questions to consider — Answers to the following questions are used to guide the long-term evaluation and management of children who present with VT:

Is the tachycardia persistent or does it recur frequently?

How long do episodes of tachycardia last, and is the child symptomatic during the episodes? Concerning symptoms include irritability and poor feeding in infants and syncope, aborted sudden death, or signs of decreased cardiac output in older children during the events.

Is there evidence of cardiac disease or dysfunction?

In children with cardiac disease, what is the natural history of the specific underlying disorder? Is there an increased risk of sudden cardiac death or life-threatening arrhythmias?

Evaluation for underlying cardiac disease — After the resolution of VT, evaluation is focused upon detecting underlying cardiac disease. Patients who are symptomatic and/or have recurrent episodes require more extensive evaluation as they are at higher risk for underlying cardiac disease. All children with even a single episode of VT should be referred to a pediatric cardiologist for evaluation and management.

The initial evaluation that should be performed in all children with VT includes electrocardiography (ECG) and echocardiography:

Echocardiography should be performed to evaluate cardiac structure and function.

Analysis of ECG while the patient is in sinus rhythm may identify many cardiac disorders associated with wide QRS complex tachycardia based upon their characteristic ECG findings. These include long QT syndrome, short QT syndrome, and, sometimes, arrhythmogenic right ventricular cardiomyopathy (ARVC; also called simply arrhythmogenic cardiomyopathy) and Brugada syndrome, all of which are associated with early sudden cardiac death and require further evaluation and therapy. (See "Causes of wide QRS complex tachycardia in children".)

In our practice, additional diagnostic studies are performed in the following circumstances:

Patient's diagnosis remains uncertain after the noninvasive evaluation above

Patient is symptomatic during episodes of VT

Patient has recurrent episodes of VT

A family history of unexpected early death

Catheter ablation is being considered

Additional testing may include magnetic resonance imaging, cardiac catheterization, 24-hour Holter monitoring, exercise and electrophysiologic testing, and genetic testing for possible underlying etiologies (eg, channelopathies, ARVC, catecholaminergic polymorphic VT [CPVT]) [18]. However, indications and utilization of each test vary among centers. (See "Causes of wide QRS complex tachycardia in children", section on 'Ventricular tachycardia'.)

Treatment — The decision to treat is influenced by the patient's age, symptoms, evidence of structural heart disease, family history, specific VT diagnosis, and electrical and hemodynamic impact of the arrhythmia. Many patients have a benign clinical course and, after a thorough evaluation, may not require therapy.

The management principles described below are generally consistent with the 2014 guidelines of the Pediatric and Congenital Electrophysiology Society and the Heart Rhythm Society on VT management in the child with a structurally normal heart [18].

Symptomatic and high-risk patients — Treatment is indicated in patients who are symptomatic or have a disease associated with a high risk of sudden cardiac death (eg, long QT syndrome, CPVT, Brugada syndrome, hypertrophic cardiomyopathy, ARVC, myocarditis). Treatment options for chronic management of VT include drug therapy, catheter or surgical ablation, left cardiac sympathetic denervation, and/or placement of an ICD [19-21]. Drug therapy should be tailored to the specific VT diagnosis, and one must consider the impact of the medication on cardiac function, especially in those with structural or functional cardiac disease. In some circumstances, especially in patients at high risk for sudden cardiac death, medications are ineffective and ICD implantation is required. These conditions are discussed in separate topic reviews:

Long QT syndrome (see "Congenital long QT syndrome: Treatment")

CPVT (see "Catecholaminergic polymorphic ventricular tachycardia")

Brugada syndrome (see "Brugada syndrome or pattern: Management and approach to screening of relatives", section on 'High-risk patients')

Hypertrophic cardiomyopathy (see "Hypertrophic cardiomyopathy in children: Management and prognosis", section on 'Prevention of sudden cardiac death (ICD placement)')

ARVC (see "Arrhythmogenic right ventricular cardiomyopathy: Treatment and prognosis")

Patients with underlying congenital heart disease — Arrhythmias, including VT, are seen as a late complication in children and adults with congenital heart disease (CHD) and are associated with a significant increase in mortality and serious morbidity. (See "Causes of wide QRS complex tachycardia in children", section on 'Congenital heart disease'.)

Symptomatic patients – Among pediatric cardiologists, there is general consensus that patients with sustained VT and/or symptoms require treatment. Treatment includes correction of residual hemodynamic defects and arrhythmia management, which may include drug therapy, catheter or surgical ablation, and/or placement of an ICD. For patients with a high burden of ventricular ectopy, medications are often inadequate and catheter ablation and/or ICD implantation may be warranted.

ICD implantation – ICD implantation is indicated in most patients with CHD who experience cardiac arrest due to VT or who have sustained hemodynamically unstable VT where a reversible cause is not identified. (See "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy".)

The decision to implant an ICD for other indications is less clear, and appropriate patient selection for primary prevention ICD implantation remains a challenge.

In our center, the decision to proceed with ICD implantation is individualized to the patient, taking into account the following considerations:

-Is there evidence of ventricular systolic or diastolic dysfunction?

-Does the patient have single-ventricle physiology?

-Are there New York Heart Association class II or III symptoms?

-Does the patient have an underlying diagnosis that puts them at high risk of recurrent ventricular ectopy and/or sudden cardiac death (eg, tetralogy of Fallot)?

-Does the patient have RV scarring from previous surgery?

-Is there a history of nonsustained VT?

-Is there inducible VT at electrophysiology testing?

-Is the QRS duration ≥180 milliseconds (in high-risk patients, >140 milliseconds)?

-Are there findings of complex ventricular arrhythmias?

-Is there a history of unexplained syncope?

-Is the patient awaiting heart transplantation?

Cardiac resynchronization therapy (CRT) – CRT has an emerging role in preserving ventricular function in the CHD population with decreased systemic ventricular function [22,23]. Although the application of this technology in adult heart failure has fairly clearly defined indications, the heterogeneity of the population has made establishing definitive guidelines difficult in CHD patients [24]. Electromechanical dyssynchrony with an underlying activation delay due to bundle branch block or in the setting of chronic ventricular pacing is the target for CRT therapy. In adult patients with systolic heart failure, CRT can lead to restoration of normal or near-normal electromechanical activation, improve myocardial efficiency, and reverse structural and cellular remodeling [25]. Despite the diverse disease processes in the CHD population, there is increasing evidence for a role for this technology [22,23,26,27]. These retrospective studies and case series involve a heterogeneous CHD population and were not randomized; thus, it is difficult to assess the impact of CRT on outcomes. Nonetheless, reverse ventricular remodeling effects appear to be similar to what is seen in adult ischemic and idiopathic cardiomyopathy populations [28]. (See "Cardiac resynchronization therapy in heart failure: Indications and choice of system", section on 'Rationale for CRT'.)

Ablation – Catheter ablation has been successful in treating ventricular arrhythmias [29-33]. RV outflow tract (RVOT) tachycardia and idiopathic left ventricular tachycardia (ILVT) are usually hemodynamically stable. In this setting, inducible monomorphic VT can be successfully induced and mapped and may be amenable to catheter ablation. In symptomatic patients with ILVT and RVOT, studies involving adult patients suggest a higher rate of success from ablation compared with pharmacologic therapy with low complication rates. Thus, catheter ablation is the preferred therapy in suitable patients [34]. (See "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis", section on 'Radiofrequency catheter ablation' and "Ventricular tachycardia in the absence of apparent structural heart disease", section on 'Radiofrequency ablation'.)

LV outflow tract (LVOT) tachycardia is often more complex and, on rare occasions, may require an epicardial approach. (See "Ventricular tachycardia in the absence of apparent structural heart disease", section on 'Epicardial ablation'.)

In the adult CHD population, ventricular ectopy and nonsustained VT are relatively common. However, sustained monomorphic VT, the most tractable target for mapping and catheter ablation, appear to be rare [28]. In a large case series of 97 patients with CHD, the overall success rate of ablation was 61 percent. In addition, in a small case report, successful ablation using three-dimensional substrate mapping during sinus rhythm was reported in 11 patients with VT after repair of CHD [32]. Although ablation may decrease the risk of subsequent VT in patients with inducible monomorphic VT, recurrences are common. Ablation has not been shown to reduce the risk of sudden death, which, in the adult CHD population, is estimated at 0.1 to 0.2 percent per year [35]. (See "Overview of catheter ablation of cardiac arrhythmias".)

Asymptomatic patients – It is unclear whether treatment is beneficial to patients with CHD who have ventricular ectopy identified on routine surveillance monitoring without associated symptoms. The clinician must balance the side effects of therapy or complications of therapeutic interventions against the risk of a life-threatening arrhythmia. Management depends upon the underlying cause of VT, local expertise and experience, medical costs, and available technology of the medical center. In our center, the decision for intervention is based upon the patient's cardiac diagnosis and his/her risk of sudden cardiac death. All patients with a high burden of ectopy are monitored for the development of arrhythmia-induced cardiomyopathy. (See 'Monitoring' below.)

Asymptomatic patients without cardiac disease — Patients who lack a worrisome family history and who have a normal resting heart rate, normal ECG, and normal cardiac structure and function on echocardiography or advanced cardiac imaging generally have a benign clinical course, and the arrhythmia either resolves spontaneously or declines over time [18,36]. For these patients, we suggest no therapeutic intervention but close monitoring, including monitoring for arrhythmia-induced cardiomyopathy in children with a high burden of ectopy. (See 'Monitoring' below.)

Infants — In the absence of structural heart disease and severe symptoms, most infants with isolated VT can be managed with observation. Isolated VT presenting in infants is often discovered as an incidental finding. Management should be based on review of the impact on the infant's growth and development [18]. A retrospective multicenter study of nearly 100 pediatric patients with VT reported that compared with children >1 year old, infants with VT are less likely to experience symptoms (22 versus 38 percent) and more likely to have complete resolution (89 versus 56 percent) [37]. Similarly, a single-center review of 31 infants with isolated VT found that all infants who were asymptomatic with a structurally normal heart and no additional electrophysiologic diagnosis had spontaneous resolution of tachycardia [36]. The time to resolution of VT was similar between infants who received outpatient antiarrhythmic medications and those who did not.

Monitoring — Patients with incessant VT or frequent ventricular ectopy (ie, >10 percent ectopic beats) are at risk for developing arrhythmia-induced cardiomyopathy and should have routine surveillance of ventricular function [18]. In our practice, we perform echocardiography every one to two years. More frequent and/or earlier re-evaluation is warranted for patients with a high burden of ectopy typically and those with new onset of symptoms or signs of heart failure. In addition, patients' development of heart failure symptoms should prompt consideration of treatment with ablation or pharmacologic therapy, as discussed above. (See 'Symptomatic and high-risk patients' above.)

In pediatric patients with evidence of diminished LV function due to VT or frequent ventricular ectopy, management should include medical or ablative options to diminish the arrhythmia burden [18]. Following restoration of sinus rhythm or ventricular rate control, most patients have significant improvement and/or normalization of ventricular function [38]. (See "Causes of wide QRS complex tachycardia in children", section on 'Arrhythmia-induced cardiomyopathy' and "Arrhythmia-induced cardiomyopathy".)

Sports participation — Sports participation in patients with VT is highly disease dependent. This issue is discussed separately. (See "Athletes with arrhythmias: Treatment and returning to athletic participation", section on 'Ventricular arrhythmias'.)

Supraventricular tachycardia — The chronic management of supraventricular tachycardia (SVT) is discussed in detail separately. (See "Management of supraventricular tachycardia (SVT) in children", section on 'Treatment to prevent supraventricular tachycardia recurrences'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Arrhythmias in children" and "Society guideline links: Basic and advanced cardiac life support in children".)

SUMMARY AND RECOMMENDATIONS

Acute management – In children who present with tachyarrhythmia, assessing and stabilizing the hemodynamic status takes precedence over the diagnostic evaluation (see 'Initial management' above):

Pulseless arrest – A patient who is unresponsive or pulseless is in cardiac arrest, and requires immediate cardiopulmonary resuscitation according to standard resuscitation algorithms (algorithm 1). (See "Pediatric advanced life support (PALS)", section on 'Pulseless arrest algorithm'.)

Unstable with a pulse – In patients who are unstable (those with palpable pulses but with poor perfusion) with wide QRS tachycardia, we recommend synchronized cardioversion (0.5 joules to 1 joule per kg) as the initial intervention (Grade 1C). In conscious patients, sedation should be provided for the cardioversion if it does not delay procedure. (See 'Initial treatment' above.)

Shock-resistant tachyarrhythmia – For pediatric patients with shock-resistant wide QRS complex tachyarrhythmia, we suggest lidocaine rather than other agents as the first-line antiarrhythmic agent (Grade 2C). The initial bolus dose of lidocaine is 1 mg/kg intravenously (IV), which may be followed by an infusion of 20 to 50 mcg/kg per minute. If the rhythm is consistent with torsades de pointes (waveform 1A-B), IV magnesium at a dose of 25 to 50 mg/kg (maximum dose 2000 mg) should be given. (See 'Shock-resistant tachyarrhythmia' above and 'Torsades de pointes' above.)

Stable patients – Management of stable patients with wide QRS complex tachyarrhythmia should be carried out in consultation with a pediatric cardiologist/electrophysiologist. Stable patients should undergo evaluation to determine the type of the arrhythmia and the underlying cause. Management depends on the type of arrhythmia:

-Ventricular tachycardia (VT) – If an underlying VT diagnosis is established, treatment is tailored to the specific diagnosis. For patients without an apparent underlying VT diagnosis, we suggest lidocaine rather than other agents for acute termination of the arrhythmia (Grade 2C). Synchronized cardioversion under sedation is another option for terminating VT in stable patients. (See 'Ventricular tachycardia' above.)

-Supraventricular tachycardia (SVT) – Stable patients with SVT and aberrant conduction resulting in wide QRS complex tachycardia are managed in the same manner as other patients with SVT, as summarized in the table (table 3) and discussed separately. (See "Management of supraventricular tachycardia (SVT) in children", section on 'Acute management'.)

Initial evaluation – Once the patient is stable, the initial evaluation in children with wide complex tachycardia includes a history, physical examination, electrocardiogram (ECG), echocardiogram, and laboratory tests, including serum electrolytes. (See 'Initial evaluation' above.)

Detailed ECG analysis determines the nature of the underlying arrhythmia and guides specific therapy. Wide QRS tachycardia with atrioventricular (AV) dissociation establishes VT as the underlying mechanism of the arrhythmia (waveform 2). (See 'Electrocardiography' above.)

Evaluation for underlying cardiac disease – After the acute episode of VT is terminated, patients should be evaluated to detect underlying cardiac disease. The assessment includes echocardiography (if not already performed) and an ECG analysis while the patient is in sinus rhythm.

Additional testing is generally warranted if:

The diagnosis remains uncertain after the initial noninvasive evaluation

The patient is symptomatic during episodes of VT

The patient has recurrent episodes of VT

There is a family history of unexpected early death

Catheter ablation is being considered

The diagnostic evaluation is tailored to the patient's clinical presentation. Testing may include cardiac magnetic resonance imaging, cardiac catheterization, 24-hour Holter monitoring, exercise and electrophysiologic testing, and/or genetic testing. (See 'Evaluation for underlying cardiac disease' above.)

Chronic management of VT – The decision for further intervention after termination of an acute episode of VT is based on the risk of sudden cardiac death (SCD). Contributing factors in decision-making include the presence of symptoms, evidence of structural or functional heart disease, family history, specific VT diagnosis, and the electrical and hemodynamic impact of the arrhythmia. (See 'Treatment' above.)

Symptomatic and high-risk patients – Patients who are symptomatic or have a disease associated with a high risk of SCD generally require treatment. Treatment options include drug therapy, catheter or surgical ablation, and/or placement of an implantable cardioverter-defibrillator (ICD). The choice of treatment is dependent upon the underlying diagnosis and the local expertise and availability at each center. (See 'Symptomatic and high-risk patients' above.)

Patients with congenital heart disease (CHD) – For individuals with repaired CHD who suffer a cardiac arrest due to VT without an identified reversible cause, we recommend ICD implantation (Grade 1B). (See "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy".)

It is unclear whether patients with CHD who present with evidence of ventricular ectopy without associated symptoms benefit from treatment. In our center, the decision for intervention is based upon the patient's cardiac diagnosis, risk of SCD, and the values and preferences of the patient and family. (See 'Patients with underlying congenital heart disease' above.)

Asymptomatic low-risk patients – In asymptomatic children with a normal resting heart rate, normal ECG, and normal cardiac structure and function and without a worrisome family history, we suggest close monitoring rather than therapeutic intervention (Grade 2C). (See 'Asymptomatic patients without cardiac disease' above.)

Monitoring – All patients with a high burden of ventricular ectopy are monitored for the development of arrhythmia-induced cardiomyopathy. (See 'Monitoring' above.)

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Topic 5758 Version 27.0

References

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