Ventricular Tachycardia

Basics

Description

  • Ventricular tachycardia (VT) is a series of 3 or more repetitive beats originating from the ventricle at a rate faster than the upper limit of normal for age. It usually is a wide complex rhythm but can appear narrow in infants, and the QRS complex is always different from sinus rhythm. VT may, but not always, have atrioventricular (AV) dissociation.
  • Sustained VT: lasts >30 seconds
  • Nonsustained VT: lasts from 3 beats to 30 seconds
  • VT may be monomorphic or polymorphic.
  • Torsades de pointes: a polymorphic variant
  • The QRS complexes gradually change shape and axis throughout the tachycardia.
  • Associated with congenital long QT syndrome, acquired long QT, and Brugada syndrome
  • Premature ventricular contractions (PVCs) have been reported in 0.8–2.2% of otherwise healthy children.

Genetics

  • Long QT syndrome may be inherited in an autosomal recessive or autosomal dominant pattern. It is related to a variety of cardiac ion channel defects and may be associated with hearing loss and/or a family history of sudden death.
  • Brugada syndrome is most commonly related to a defect in the cardiac sodium channel (SCN 5A) and appears to be inherited in an autosomal dominant pattern.

Pathophysiology

VT may result from a reentrant mechanism, triggered mechanism, or abnormal automaticity.

Etiology

  • Diverse and often overlapping
  • Idiopathic
  • Myocarditis or dilated cardiomyopathy
  • Long QT syndrome (LQTS)
  • Right ventricular dysplasia
  • Brugada syndrome
  • Before and after surgery for congenital heart disease (e.g., tetralogy of Fallot, transposition of the great arteries, aortic stenosis, hypertrophic cardiomyopathy, myocardial tumors, Ebstein anomaly, and pulmonary vascular occlusive disease)
  • Metabolic disturbances (hypoxia, acidosis, hypo/hyperkalemia, hypomagnesemia, hypothermia)
  • Drug toxicity (e.g., digitalis toxicity, antiarrhythmic agents)
  • Substance abuse (cocaine, methamphetamine)
  • Myocardial ischemia (e.g., Kawasaki disease, congenital coronary anomalies)
  • Trauma
  • Invasive lines or catheters
  • Pericardial effusion
  • Catecholaminergic polymorphic VT

Diagnosis

Based on electrocardiogram (ECG), rhythm strip, Holter, or event monitor

History

  • Varies widely, ranging from asymptomatic to sudden cardiac arrest/death
  • Other symptoms include palpitations, presyncope or syncope, exercise intolerance, and dizziness.

Physical Exam

  • Can be normal; occasional heart rhythm irregularity secondary to frequent PVCs
  • Acute, sustained VT may have signs of hemodynamic compromise, including lack of pulse.
  • Signs of underlying heart disease, if any, are present.

Diagnostic Tests and Interpretation

Lab

  • Serum electrolytes, including magnesium and potassium levels, blood gas, and serum drug levels as appropriate
  • Urine toxicology screen
  • ECG
    • ≥3 consecutive ventricular complexes faster than the upper limit of normal for age
    • Bundle branch morphology (right or left) may indicate the site of origin of the VT. May have AV dissociation
    • Typically, repolarization (T-wave) abnormalities are present.
    • The QTc interval should be measured in lead II during sinus rhythm.
    • Evaluate for Brugada syndrome in leads V1 and V2 (right bundle branch block, coved-type ST elevation, and T-wave inversion in the right precordial leads). Brugada syndrome ECG findings may be more obvious when the patient is febrile.
  • Echocardiogram
  • Rule out congenital heart disease (CHD), pericardial and pleural effusions, tumors, and hypertrophic cardiomyopathy and assess ventricular function.
  • Cardiac magnetic resonance imaging may be helpful in addressing abnormalities that are beyond the resolution of echocardiography.
  • Ambulatory Holter monitor
  • Quantitative assessment of ventricular ectopy, and frequency of VT
  • Less frequent episodes may need an event monitor or loop recorder.
  • Exercise stress test (>5 years old)
    • Benign PVCs are characteristically suppressed with exercise and return in the immediate recovery period.
    • Exacerbation or worsening of ventricular arrhythmias is concerning.
  • Cardiac catheterization: assessment of hemodynamics, endomyocardial biopsy, and coronary artery angiography
  • Electrophysiologic study indications
    • Confirm diagnosis and mechanism of a wide complex rhythm.
    • Evaluate suspected VT in the setting of structural or functional heart disease, syncope, or cardiac arrest.
    • Evaluate nonsustained VT in patients with CHD.
    • Determine appropriate medical therapy in a patient with inducible VT.
    • Evaluate syncope in the setting of palpitations (SVT vs. VT).
    • Characterize VT with consideration for catheter ablation.
      • Note: Electrophysiologic studies are generally not helpful in individuals with LQTS.

Differential Diagnosis

Wide complex tachyarrhythmia

  • Should always suspect VT until proven otherwise
  • Supraventricular tachycardia (SVT) with aberrancy
  • Antidromic tachycardia (antegrade conduction down an accessory pathway during an AV reciprocating tachycardia (e.g., Wolff-Parkinson-White syndrome)
  • Atrial flutter or fibrillation with rapid antegrade conduction over an accessory pathway

Treatment

  • Acute
    • If the patient is hemodynamically compromised, prompt synchronized direct-current (1–2 joules/kg; adult, 100–400 joules) cardioversion is indicated.
    • Asynchronous cardioversion for ventricular fibrillation or pulseless VT
    • Cardiopulmonary resuscitation as necessary
    • Lidocaine (1 mg/kg bolus over 1 minute, followed by an infusion at 20–50 μg/kg/minute, assuming normal liver and kidney function)
    • If torsades de pointes, MgSO4 may be given
    • Overdrive ventricular pacing may terminate the tachycardia; however, pacing may accelerate the VT or induce ventricular fibrillation.
    • IV amiodarone (side effect: hypotension, responds to volume)
  • Chronic
    • Medications
      • Class IB (mexiletine and phenytoin). β-Blockers (propranolol, atenolol, nadolol) are used in LQTS and may be effective in exercise-induced VT and postoperative CHD.
      • Class III agents (amiodarone and sotalol) should be avoided in patients with LQTS.
      • Class IC agents (flecainide) may be proarrhythmic, and sudden death has been reported in patients with structural heart disease who were taking class IC agents.
      • Verapamil for right ventricular outflow tract VT and verapamil-sensitive left ventricular VT
    • Atrial pacing at rates slightly faster than VT rates may suppress tachycardia.
    • Catheter ablation using radiofrequency energy or cryoenergy
    • Implantable cardioverter defibrillators

Ongoing Care

Prognosis

  • Generally very good in patients with idiopathic VT and a structurally normal heart.
  • Suppression of ventricular ectopy with exercise has a favorable prognosis.
  • In patients with heart disease (congenital or acquired) or LQTS, VT may increase the risk of presyncope, syncope, and possibly sudden death.

Complications

  • Cardiovascular compromise (sudden death)
  • Acquired cardiomyopathy (from long-standing VT and a lack of AV synchrony)

Patient Monitoring

  • Depends on the underlying cause
  • ECG, Holter monitor, and exercise stress test

Additional Reading

  1. Gilbert-Barness E, Barness LA. Pathogenesis of cardiac conduction disorders in children: genetic and histopathologic aspects. Am J Med Genet A. 2006;140(19):1993–2006.  [PMID:16969859]
  2. Hebbar AK, Hueston WJ. Management of common arrhythmias: part II. Ventricular arrhythmias and arrhythmias in special populations. Am Fam Physician. 2002;65(12):2491–2496.  [PMID:12086238]
  3. Kleinman ME, Chameides L, Schexnayder SM, et al. Part 14: pediatric advanced life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(18)(Suppl 3):S876–S908.  [PMID:20956230]
  4. Sarubbi B. The Wolff-Parkinson-White electrocardiogram pattern in athletes: how and when to evaluate the risk for dangerous arrhythmias. The opinion of the paediatric cardiologist. J Cardiovasc Med (Hagerstown). 2006;7(4):271–278.  [PMID:16645401]
  5. Wren C. Cardiac arrhythmias in the fetus and newborn. Semin Fetal Neonatal Med. 2006;11(3):182–190.  [PMID:16530495]
  6. Yabek SM. Ventricular arrhythmias in children with an apparently normal heart. J Pediatr. 1991;119(1, Pt 1):1–11.  [PMID:2066839]

Codes

ICD-9

  • 427.1 Paroxysmal ventricular tachycardia
  • 26.82 Long QT syndrome
  • 746.89 Other specified congenital anomalies of heart

ICD-10

  • I47.2 Ventricular tachycardia
  • I45.81 Long QT syndrome
  • Q24.8 Other specified congenital malformations of heart

SNOMED

  • 25569003 Ventricular tachycardia (disorder)
  • 9651007 Long QT syndrome (disorder)
  • 418818005 brugada syndrome (disorder)
  • 426525004 sustained ventricular tachycardia (disorder)
  • 444658006 Nonsustained ventricular tachycardia

FAQ

  • Q: Do frequent single PVCs require treatment?
  • A: In an otherwise healthy child with a structurally normal heart, normal QT interval, and PVCs that suppress with exercise, no treatment is indicated.
  • Q: Should siblings of patients with LQTS be evaluated?
  • A: Yes. Siblings and parents (even if asymptomatic) should have an ECG, Holter monitor, and exercise stress test for definitive evaluation of the QT interval. Commercial genetic testing is currently available to detect mutations in some of the most common genes that cause the LQTS. The test will positively identify ∼75% of patients with the LQTS. Genetic testing may be considered in patients in whom there is a high suspicion of LQTS.

Authors

Arvind Hoskoppal


© Wolters Kluwer Health Lippincott Williams & Wilkins

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