eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Ventricular Tachycardia

Author: Mark E Alexander, MD, Assistant Professor, Department of Pediatrics, Children's Hospital of Boston and Harvard Medical School
Coauthor(s): Charles I Berul, MD, Associate Professor of Pediatrics, Harvard Medical School; Senior Associate, Department of Cardiology, Children's Hospital of Boston
Contributor Information and Disclosures

Updated: Feb 3, 2009

Introduction

Background

Ventricular arrhythmia (VA) may be an isolated and completely benign finding in children, a marker of serious systemic disease or myopathy, or a mechanism for sudden cardiac death (SCD) and syncope.

Isolated premature ventricular contractions (PVCs) are reasonably common. They occur with low daily frequency in as many as 40% of patients with apparently normal hearts.1,2,3,4 PVCs occur with increased frequency in more than 60% of patients with some types of repaired congenital heart disease (CHD). By comparison, sustained VA is much less frequent. Although sustained VA can occur in apparently normal hearts, approximately 50% of patients have either CHD or myopathy. An increasingly sophisticated molecular understanding of the role of electrical myopathies, including ion-channel defects such as long QT syndrome (LQTS), offers increased insight into the nature of some of these diseases.

Clinical choices regarding imaging and therapy primarily focus on the potential mortality risks associated with the specific clinical setting. The incidence of SCD in pediatric patients is low. Even among patients with known heart disease, consider the potential risks of potent antiarrhythmic medications and of nonpharmacologic therapy (eg, catheter ablation, implantable antitachycardia pacemakers and/or defibrillators). Even with the low incidence of sudden death in pediatric patients, clinical decisions are often difficult.

Pathophysiology

Reentrant, automatic, or triggered mechanisms may cause VA, just as these mechanisms cause supraventricular tachycardia (SVT) and other arrhythmias. Each of these mechanisms can occur in structurally and functionally normal hearts. Both myopericarditis and many forms of cardiomyopathy increase the potential for VAs. Myocardial tumors result in mechanical stresses that facilitate arrhythmias.

Reentrant arrhythmia

Reentrant arrhythmia depends on a circuit, often caused by surgical scar, fibrosis, or fatty degeneration. These areas of functionally abnormal tissue foster the conditions necessary for reentry. These conditions permit a zone of slow conduction, a line of functional unidirectional block, and a circuit that allows circus rhythm to continue. Pediatric patients with surgical ventricular scars, such as those with postoperative ventricular tachycardia (VT) after repair of tetralogy of Fallot, are commonly cited examples of this mechanism. Chaotic rhythms (eg, ventricular fibrillation) are also examples of reentry mechanisms. In clinical practice, reentrant rhythms are triggered by premature beats, and the tachycardia is often terminated with direct-current (DC) cardioversion. An abrupt onset and a generally stable rate are other characteristics of reentrant rhythms.

Automatic rhythms

Automatic rhythms are more common than reentrant rhythms in pediatric patients with apparently normal hearts and are caused by abnormal cellular automaticity. The most frequent automatic rhythm is caused by increased spontaneous depolarization of phase 4 of the cardiac action potential. Abnormal automaticity, in turn, may be the result of metabolic derangement, or the automaticity may be idiopathic. Metabolic derangements that may result in abnormal automaticity include hypokalemia, hypomagnesemia, and local cellular abnormalities that may include inflammation from myocarditis. High atrial rates suppress, but do not eliminate, automatic VT. These rates vary with the autonomic state, often in complicated fashions. A benign accelerated idioventricular rhythm is an example of an autonomic mechanism.

At a cellular level, ion-channel defects, such as LQTS, allow abnormal cellular automaticity to trigger potentially fatal polymorphic VT, also known as torsade de pointes. Triggered arrhythmia may also play a role in poisoning by antiarrhythmic drugs (eg, digoxin).

Frequency

United States

The frequency of VA entirely depends on the underlying substrate.

Large pediatric referral centers may encounter 3-5 patients with sustained VT each year.5  The incidence of low-grade ectopy is notably increased in patients with CHD or cardiac myopathies. Among patients with CHD, this incidence is concentrated among those who have had ventricular incisions (eg, ventricular septal defects, D-transposition with ventricular septal defects, tetralogy of Fallot) and aortic stenosis; as many as two thirds of patients in this population have some ectopy. This incidence appears to be increased in older patients, probably among those undergoing repair relatively late in life and with techniques used before the mid 1980s.

Although individual underlying myopathies are rare, each contributes to the overall incidence of VA. Hypertrophic cardiomyopathy (HCM) is most common, with a frequency as high as 0.02-0.2% of the population, although the population-based frequency among young people is generally lower.6 Ion-channel defects (eg, LQTS) are less common; the frequency is difficult to quantitate but is probably approximately 1 case per 5000-10,000 persons. Despite the rarity of these conditions, each has an annual mortality risk as high as 3-5%.

International

The etiology of VA varies internationally. Chagas disease (trypanosomiasis) is an epidemic cause of dilated cardiomyopathy in Brazil and in other regions of South America.

In Europe, a heritable arrhythmogenic right ventricular dysplasia (ARVD) may be a leading cause of sudden death and VT in young people, particularly younger adults. The difference in perceived frequency likely results from a combination of genetic factors, variable definitions of ARVD, and differences in regional recognition of this entity.

Mortality/Morbidity

The overwhelming majority of pediatric patients evaluated for nonsustained VA have no symptoms or nonspecific palpitations. Obvious concerns include risk of cardiac syncope or SCD. This risk is low, except in selected patients with organic heart disease, for whom the annual risk of sudden death may be as high as 3% for those with sustained VT. The frequency distribution of sudden death in CHD overlaps with that of ventricular ectopy (see Media file 1).

Much concern regarding VA focuses on identifying preventable causes of SCD. The annual incidence of SCD in most clinically defined subgroups of pediatric patients is low. Nonselected pediatric populations have exceptionally low mortality rates (approximately 1-5 deaths per 100,000 patient-years). In contrast, the annual sudden death rate in the general adult population is 1-3 deaths per 1000 patient-years; the annual mortality rate in adult survivors of myocardial infarction with depressed ventricular function and inducible, nonsuppressible VT is 20%. For older patients with palliated heart disease or genetic arrhythmias, the risks are higher, although the rate is still usually no more than 1-3% annually. Issues of predicting low-frequency disease—difficult issues in any setting—are magnified in the population with CHD and particularly in the overall pediatric population.

Among infants and children with minimal symptoms and normal ventricular function (and even very frequent VA, including VT), most have spontaneous resolution of their arrhythmia, with little intercurrent morbidity.7,8,9,10,11

Race

Data about the influence of race in pediatric SCD are limited. Incidences of some heritable myopathies vary by ethnic group. Despite these variations, most diagnoses should be considered in all ethnic groups. The incidence of LQTS appears to be decreased in blacks, and ARVD appears most frequent in patients of southern European ancestry. Although Brugada syndrome has been identified in many ethnic groups, it is identical to the sudden unexpected nocturnal death syndrome identified in men of Southeast Asian ancestry.

Sex

No significant sex differences have been reported in overall incidence or severity of VA, though patterns of distribution of different LQTS genotypes may vary by sex. In addition, the implications of LQTS, HCM, ARVD, and other genetic cardiac defects appear to have some sex specificity.

Age

Population-based studies in children have been relatively small but demonstrated a biphasic peak of simple ventricular ectopy in apparently healthy infants. This rate decreases during preschool and elementary school ages and increases with adolescence. As patients move into adult life, the incidence of ventricular ectopy continues to steadily increase (see Media file 2). Although as many as 15% of infants and 40% of adolescents have infrequent ventricular ectopy, high-grade ectopy and VT are notably infrequent.

The incidence of VA is somewhat bimodal in patients without structural heart disease. Infants and adolescents have more cases of VA than do toddlers and younger school-aged children. The nature and classification of these cases also differs with age.

In patients with repaired CHD, incidence of VA is notably increased among older adolescents and young adults. This increase may reflect the management approach taken when these patients were younger, the long period after open-heart repair, and/or the influence of autonomic changes on the heart during adolescence.

Clinical

History

  • The following historical details raise particular concern for ventricular arrhythmia (VA):
    • Presence and severity of symptoms
    • Presence of symptoms with exercise
    • Previous cardiac diagnoses and procedures
    • Family medical history suggestive of inherited disease
    • Potential for recent medication or recreational drug use
  • In the pediatric population, neurally mediated syncope is so common—and life-threatening arrhythmia is so rare—that investigations of VA in patients with syncope are often unrevealing. Details of the history and family history can direct additional, extensive investigation. Diagnostic findings such as "class II" genetic mutations, which may represent pathologic findings, or nonreproducible findings during intracardiac studies may represent false-positives.
    • A family history of sudden death before age 40 years should raise suspicions, even if the cause was an apparent accident.
    • Numerous familial low-incidence cardiomyopathies have arrhythmia as an important symptom. These cardiomyopathies are characterized by several phenotypes and variable penetrance.
    • When a potentially genetic disorder is identified, careful family investigation can identify other affected families members. The reported yields vary but may approach 50%.  
  • Precipitating events may include the following:
  • Syncope
    • Apparent cardiac syncope consistently increases the potential of identifying a life-threatening disease that requires active management.
    • Cardiac syncope, in contrast to typical neurally mediated syncope, is characterized by abrupt onset associated with exercise, clinically significant injury, incontinence, seizure, and rapid recovery when arrhythmia is transient.
    • Palpitations are common in neurally mediated syncope and in cardiac syncope. During benign episodes, these palpitations are often described as hard beats at lower rates, compared with the rapid pulse identified when tachycardia triggers syncope.
    • Syncope in the presence of known or apparent heart disease should be presumed to represent a potentially serious arrhythmia until proven otherwise.
    • A new presentation of syncope and VAs may be particularly worrisome.
  • Near-syncope or dizziness
    • The vast majority of patients with episodic dizziness, light-headedness, or other presyncopal symptoms have benign or self-limited diagnoses.
    • Clinical correlation is critical when presyncopal symptoms are associated with ventricular ectopy or other arrhythmia.
  • Palpitations
    • Patients with isolated premature ventricular contractions (PVCs) and those with sustained arrhythmia may report symptomatic palpitations. Particularly with PVCs, the postextrasystolic beat may have an increased stroke volume.
    • Of note, many patients do not report any symptoms and cannot identify when they are having ventricular beats. As in patients with syncope, palpitations frequently occur in patients without significant arrhythmia. Ambulatory ECGs (eg, those recorded with Holter or memory-looping event monitors) are critical tools to correlate symptoms and rhythm.
  • Chest pain
    • Most chest pain is clearly of musculoskeletal origin (costochondritis); physical examination reveals reproducible point tenderness and no clinical suggestion of heart disease.
    • Another common scenario is atypical chest pain, which is described as brief, sharp, and stabbing. This finding is poorly correlated with exercise and not correlated with the ECG.
    • Chest pain may represent a marker of hypertrophic cardiomyopathy (HCM) or relatively common diagnoses.
    • Typical angina is extremely rare.
    • Sudden cardiac death (SCD) and rare cases of coronary artery disease are clearly related in some way. VA may be secondary to Kawasaki disease, congenital coronary anomalies, or typical angina.
    • Pediatric chest pain, is typically poorly defined and may include arrhythmia symptoms, pulmonary symptoms or GI symptoms in addition to anxiety. In contrast to older adults, the serious cardiac causes of chest pain are all rare, which influences both the need for additional testing and the yield of that testing.

Physical

  • Cardiac examination
    • Perform detailed cardiac examination. Focus on clinically apparent arrhythmia and physical signs of heart failure or structural heart disease.
    • Normal results do not exclude serious or life-threatening disease.
  • General physical examination: Particularly focus on evidence of occult or apparent skeletal myopathy, neurocutaneous syndromes, rickets, and previous procedures.

Causes

Potential causes of VAs include the following:

  • Mechanical causes
    • Intraventricular catheters
    • Myocardial tumors
  • Metabolic causes
  • Drugs
    • Digoxin toxicity
    • Proarrhythmia
    • Most antiarrhythmia drugs (especially classes I-A, I-C, III)
    • Positive inotropes and chronotropes (eg dopamine, isoproterenol).
    • Other drug toxicity
    • Anesthesia
  • Inflammatory causes
  • Cardiomyopathy - Muscular dystrophy
  • Genetic causes
  • Electrical myopathy
    • Long QT
    • Brugada syndrome
    • Catecholaminergic polymorphic ventricular tachycardia (VT)
  • Structural - Congenital heart disease (CHD)
  • Neoplastic causes - Tumors (eg, rhabdomyoma)
  • Sustained and nonsustained VT
    • Sustained VT is defined as consecutive ventricular rhythm longer than 30 seconds at rates faster than 110-120 beats per minute (bpm) or a comparable arrhythmia requiring urgent cardioversion.
    • Nonsustained VT includes 3 or more consecutive beats lasting less than 30 seconds. High-grade ventricular ectopy is the VA classification that includes combinations of ventricular couplets and polyform PVCs, which are more frequent than isolated PVCs and less sustained than VT.
  • Nonstructural heart disease
    • Electrical myopathies, LQTS: This familial ion-channel defect is caused by a microdeletion; deletions in chromosomes 3, 4, 7, 11, and 21 have been identified. Although each defect is unique, they share a tendency to abnormal repolarization and an increased risk of sudden death associated with torsade de points. High-dose beta-blockade has been a mainstay therapy for years. Novel approaches with atrial pacing, implantable cardioverter/defibrillators (ICDs), and gene-specific ion-channel manipulation may help certain patients.
    • Arrhythmogenic right ventricular cardiomyopathy (ARVC): This is the most frequent diagnosis in southern Europeans who die during exercise. This complex and heterogeneous myopathy is associated with fatty degeneration of the right ventricle and inducible VA.
    • HCM: SCD, apparently mediated by VT, occurs in young people with HCM. High-grade ectopy, as shown on Holter monitoring, is an apparent risk factor for SCD in adults with HCM; however, this finding provides little assistance to pediatric patients. Correlation in genotype-positive families with HCM suggests that as many as a quarter of children and adolescents with mild or early forms of HCM may be missed during ECG screening.12 Arrhythmia and mortality risks associated with HCM widely vary. Data from population-based pediatric studies and the pediatric cardiomyopathy registry suggest that the risk for older children and adolescents with HCM is 1% per year or less.6 Infants and those with inborn errors of metabolism represent patients with notably increased risk.
    • Brugada syndrome: Brugada syndrome represents another identifiable genetic defect (of the sodium channel) that causes VAs. Patients with this syndrome tend to present with a pattern of right bundle-branch block (RBBB) on resting ECG and ST-segment elevation. Both fevers and full stomachs may be important triggers of the pattern, and fever is a frequent contributor to childhood events.13
    • Catecholaminergic polymorphic VT: This is yet another identifiable ion-channel defect that occurs on a relatively frequent familial basis, with recurrent polymorphic VT, a normal resting ECG, and normal repolarization. Genetic studies have identified patients and families with mutations in the ryanodine receptor, among other gene defects. These patients often have atrial and junctional arrhythmias along with relative sinus bradycardia.
  • Acute myocarditis
    • Acute viral myocarditis with depressed ventricular function and active inflammation, whatever the etiology, can cause ventricular ectopy and VT.
    • Short-term drug therapy to suppress arrhythmia is indicated while myocarditis is managed.
    • For the acute patient with profound ventricular dysfunction urgent transfer for consideration of mechanical support may be life-saving.  
    • Arrhythmias may persist well after the hemodynamic dysfunction has resolved.
  • Occult or focal myocarditis
    • Although infrequent, well-documented cases of focal or occult myocarditis associated with VA have clearly occurred.
    • Some patients with frequent ectopy or idiopathic VT may also have subclinical myocarditis. Functional imaging studies and endomyocardial biopsy may help identify these patients.
  • Idiopathic arrhythmias
    • Idiopathic arrhythmias have characteristic patterns but lack the diagnoses outlined above.
    • Benign arrhythmia is always diagnosed with caution on the basis of the symptoms, family history, echocardiogram, response to and rate of exercise, morphology, and persistence of the arrhythmia.
      • Isolated PVCs: Infrequent, isolated PVCs, particularly with a trigger such as anesthesia or an intracardiac catheter, require little investigation. PVCs notably more frequent than expected for the patient's age may warrant investigation to seek evidence of sustained arrhythmia.
      • Right ventricular outflow tract VT: Frequently asymptomatic, this type has a left bundle-branch block (LBBB) morphology, often-repetitive salvos of VT, possibly subtle MRI findings, and low-to-absent mortality. ARVD is often a difficult diagnostic challenge.
      • RBBB VT: This type may be automatic. Some occurrences may be reentrant VT triggered by atrial pacing or atrial premature beats. Seen in all ages, RBBB VTs often respond to verapamil therapy.
      • Accelerated idioventricular rhythm: Typically seen in infants and young children, accelerated idioventricular rhythm rates are slightly faster than sinus beats. LBBB is usually seen, suggesting a right ventricular focus. No mortality has been reported with this condition, and therapy is infrequently needed. Carefully observe affected infants for evidence of increasing VT or decreasing function.
  • Congenital heart disease
    • PVCs: These are seen in as many as two thirds of adolescents and young adults with moderate-to-severe valvar aortic stenosis or repaired tetralogy of Fallot. PVCs are also seen in some patients with ventricular septal defects and in patients with irreparable heart disease, especially those with pulmonary hypertension. Without symptoms, these findings are best interpreted by understanding the hemodynamics of the underlying illness.
    • Nonsustained and sustained VT
      • The classifications of nonsustained and sustained VT in patients with CHD are identical to those of patients with structurally normal hearts. These classifications should be considered in the context of the patient's symptoms and current hemodynamic status.
      • The presence of clinical VT and, in some settings, VT induced during electrophysiologic testing, may be independent of other hemodynamic defects in predicting the risk of cardiac arrest and mortality. Careful consultation and evaluation is appropriate. Tetralogy of Fallot, the defect most commonly associated with spontaneous or induced monomorphic VT, is strongly associated with increasing age, increasing age at initial repair, and residual hemodynamic defects. Management choices are complex and may include drug therapy, implantable cardioverters/defibrillator (ICD) therapy, ablation, or management of residual hemodynamic issues.

More on Ventricular Tachycardia

Overview: Ventricular Tachycardia
Differential Diagnoses & Workup: Ventricular Tachycardia
Treatment & Medication: Ventricular Tachycardia
Follow-up: Ventricular Tachycardia
Multimedia: Ventricular Tachycardia
References
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Further Reading

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Keywords

ventricular tachycardia, nonsustained ventricular tachycardia, accelerated ventricular rhythms, premature ventricular contractions, PVC, repetitive monomorphic ventricular tachycardia, sustained monomorphic ventricular tachycardia, torsade de pointes, ventricular ectopic activity, VEA, ventricular ectopy, ventricular fibrillation, V fib, ventricular flutter, V flutter, ventricular premature beats, ventricular arrhythmia, VA, VT, V tach, sudden cardiac death, syncope, congenital heart disease, long QT syndrome, LQTS, tetralogy of Fallot, ventricular fibrillation, aortic stenosis, hypertrophic cardiomyopathy, HCM, ventricular septal defects, Chagas disease, trypanosomiasis, Brugada syndrome, cocaine, tricyclic antidepressant use, Kawasaki disease, right bundle-branch block, RBBB, right ventricular outflow tract ventricular tachycardia, left bundle-branch block, LBBB

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Contributor Information and Disclosures

Author

Mark E Alexander, MD, Assistant Professor, Department of Pediatrics, Children's Hospital of Boston and Harvard Medical School
Mark E Alexander, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, Heart Rhythm Society, and Pediatric Electrophysiology Society
Disclosure: Nothing to disclose.

Coauthor(s)

Charles I Berul, MD, Associate Professor of Pediatrics, Harvard Medical School; Senior Associate, Department of Cardiology, Children's Hospital of Boston
Charles I Berul, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Heart Rhythm Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Christopher Johnsrude, MD, Associate Professor of Pediatrics, Director of Electrophysiology, University of Louisville School of Medicine; Consulting Staff, Pediatric Cardiology Associates, PSC
Christopher Johnsrude, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Cardiology
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Hugh D Allen, MD, Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine
Hugh D Allen, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, and Western Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Gilbert Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College
Gilbert Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD, Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin
Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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