eMedicine Specialties > Cardiology > Arrhythmias

Ventricular Tachycardia: Differential Diagnoses & Workup

Author: Steven J Compton, MD, FACC, FACP, Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals
Contributor Information and Disclosures

Updated: Oct 24, 2008

Differential Diagnoses

Accelerated Idioventricular Rhythm
Pacemaker Syndrome
Atrial Fibrillation
Pacemaker-Mediated Tachycardia
Atrial Flutter
Paroxysmal Supraventricular Tachycardia
Atrial Tachycardia
Torsade de Pointes
Long QT Syndrome
Ventricular Fibrillation
Multifocal Atrial Tachycardia
Wolff-Parkinson-White Syndrome
Pacemaker Failure

Other Problems to Be Considered

Supraventricular tachycardia, atrial ectopic tachycardia (SVT, AET) with aberrant conduction
ECG lead motion artifact
Inappropriate rate responsive pacing
Dual-chamber pacemaker tracking an atrial tachycardia

Workup

Laboratory Studies

Ventricular tachycardia at acute presentation

  • If the patient is unconscious or hemodynamically unstable, the diagnosis is made from the physical findings and ECG rhythm strip. Laboratory studies are impractical and ACLS protocols are quickly followed. If circumstances allow, a full 12-lead electrocardiogram should be obtained prior to urgent cardioversion.
  • If the patient presents with hemodynamic stability, then 12-lead electrocardiogram and electrolytes may be obtained prior to attempted conversion with medications or sedation and cardioversion. Electrocardiography is the criterion standard for diagnosis of VT.
  • Several different schemes exist to discriminate between VT and aberrantly conducted SVT. Brugada et al15 proposed ECG criteria that focused primarily on the QRS morphologies in the precordial leads (V1 -V6). VT mechanism was predicted by the following:
    • The absence of RS complexes in the precordial leads
    • RS duration greater than 100 milliseconds in any precordial lead
    • Ventriculoatrial dissociation in any of 12 leads
    • Certain QRS morphologies, such as QR or QS in V6
  • More recently, Vereckei et al16 have refined a different algorithm based upon the single lead aVR. They noted the presence of a negative QRS complex in aVR during right or left bundle branch conduction of supraventricular tachycardia (SVT). They found that VT mechanism was predicted by the following:
    • Presence of an initial R wave in aVR
    • Width of an initial r or q wave >40 ms in aVR
    • Notching on the initial downstroke of a predominantly negative QRS complex in aVR
    • Ventricular activation-velocity ratio (Vi/Vt) less than or equal to 1

Examples are as follows:

This ECG is from a 32-year-old female with recent...

This ECG is from a 32-year-old female with recent-onset congestive heart failure and syncope.

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This ECG is from a 32-year-old female with recent...

This ECG is from a 32-year-old female with recent-onset congestive heart failure and syncope.


This is a tachycardia with a 1:1 atrial:ventricular relationship. It is not clear from this tracing whether the atria are driving the ventricles (sinus tachycardia) or the ventricles are driving the atria (ventricular tachycardia). At first glance, sinus tachycardia might be considered with severe conduction disease manifesting as marked first-degree atrioventricular block with left bundle branch block. Looking more closely, ECG morphology gives clues to the actual diagnosis of ventricular tachycardia. These clues include the absence of RS complexes in the precordial leads, a QS pattern in V6, and an R wave in aVR. The patient proved to have an incessant VT associated with dilated cardiomyopathy.

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Ventricular tachycardia postconversion

  • Repeat the electrocardiogram after termination of VT to evaluate for acute or chronic infarction, ischemia, scar, ventricular preexcitation, hypertrophy, conduction disease, QT prolongation, and other precordial repolarization abnormalities (Brugada syndrome, arrhythmogenic right ventricular dysplasia).
  • Include electrolyte levels in an acute evaluation. Hypokalemia is a common VT trigger and is commonly seen in patients taking diuretics.
  • Toxicology screens for cocaine metabolites and tricyclic antidepressants in accordance with the clinical history.
  • Check cardiac enzyme levels if clinical symptoms or signs of ischemia are present. Persistently elevated cardiac enzyme levels may also be an indication of ongoing myocarditis.
  • In some patients with spontaneous polymorphic VT, genetic studies may be helpful for family screening or for clarifying a diagnosis. Commercial genotyping studies have been available in the United States since 2004. Spontaneous polymorphic VT may be related to genetic mutations affecting ion channels, as occurs in long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic VT. Finally, some patients are predisposed to drug-induced ventricular arrhythmias by otherwise subclinical genetic ion channel defects.

Imaging Studies

  • Following conversion to sinus rhythm, evaluation should usually include echocardiography and coronary angiography to assess for structural and ischemic heart disease. These considerations are paramount in defining further treatment in any patient with ventricular tachycardia (VT). These patients often require aggressive management of underlying ischemic heart disease and congestive heart failure.
  • Chest radiographs may be helpful to assess pulmonary congestion.
  • Cardiac computed tomography (CT) scans and cardiac magnetic resonance (cMR) imaging technologies are evolving quickly but have not yet supplanted echo and nuclear imaging for quantification of ventricular function. cMR can be especially helpful in the evaluation of uncommon myocardial infiltrative diseases such as sarcoidosis.
  • Although cardiac MR is often used for evaluation of arrhythmogenic right ventricular dysplasia, the diagnostic yield of this test has yet to be clearly defined. Right ventricular angiography may still be the criterion standard imaging study for arrhythmogenic right ventricular dysplasia (ARVD).

Other Tests

  • Signal-averaged ECG is a noninvasive test that often produces abnormal results in patients with ventricular tachycardia (VT) related to prior infarct or right ventricular dysplasia. T-wave alternans testing has also been proposed as a noninvasive risk stratifier for sudden death risk, but definitive studies are still lacking.
  • Occasionally, patients present with recurrent syncope or palpitations. In this setting, an arrhythmic cause of syncope may be sought. Options include Holter monitoring, which has a low yield, or event recording. The goal is to document the patient's rhythm during symptoms. If this is not practical, a provocative electrophysiologic study (EPS) can be performed.
  • The presence of a dual chamber pacemaker or implantable cardioverter-defibrillator (ICD) can occasionally simplify diagnosis. Most contemporary devices are capable of recording and logging tachyarrhythmias for subsequent analysis during interrogation of the implanted device.
  • On the other hand, patients with pacemakers and ICDs may present with wide complex tachycardia (WCT) secondary to rapid ventricular pacing.
    • Possibilities include tracking of an atrial tachyarrhythmia in a dual-mode, dual-pacing, dual-sensing (DDD) or an atrial-triggered, ventricular-inhibited (VDD) device; endless loop tachycardia; inappropriate rate responsive pacing due to sensor problems or incorrect sensor programming; and overt pacemaker failure (runaway pacer).
    • The most common problem involves the patient whose device is tracking atrial fibrillation or flutter. In the absence of a mode-switching algorithm, a VDD or DDD pacer responds by pacing the ventricle at the programmed upper rate limit of the device. Application of a magnet to the pacer generator may terminate endless loop tachycardia or drop the paced rate enough to allow diagnosis of the underlying atrial tachyarrhythmia.

Procedures

  • Diagnostic electrophysiologic study (EPS) requires placement of electrode catheters in the ventricle, followed by programmed ventricular stimulation using progressive pacing protocols. Premature ventricular beats are induced following conditioning pacing drives, in an attempt to induce reentrant arrhythmia. In patients with symptoms suggestive of ventricular tachycardia (VT), this kind of provocative testing can be used to assess whether the ventricles can sustain a reentrant tachyarrhythmia. Diagnostic yield of EPS is highest in patients with reentrant VT circuits.
  • EPS is particularly relevant to patients felt to be at high risk for sudden death due to significant underlying structural heart disease. EPS may be useful in demonstrating whether the substrate for sustained VT is present in a patient presenting with syncope or ischemic, nonsustained VT. In patients with recurrent symptoms related to VT, programmed electrical stimulation can generally reproduce clinically relevant VT circuits.
  • If right ventricle dysplasia is being considered, many laboratories perform right ventricular angiography as a part of the EPS. Diagnostic abnormalities include right ventricular dilation, dyskinesis, and aneurysms.

Histologic Findings

As noted above, most reentrant ventricular tachycardias (VTs) are related to myocardial scarring from ischemic or dilated cardiomyopathy. Fibrotic replacement of myocytes and interweaving of scar tissue with functional myocytes is common along slow conduction zones of VT circuits.

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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References

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Further Reading

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Keywords

ventricular tachycardia, VT, ischemic heart disease, ventricular fibrillation, VF, monomorphic VT, polymorphic VT, long QT syndrome, short QT syndrome, idiopathic VF, Brugada syndrome, familial adrenergic polymorphic VT, bradycardia, ischemic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, Chagas disease, right ventricular dysplasia, torsade de pointes, hypertrophic cardiomyopathy, right ventricular cardiomyopathy, myocarditis, coronary artery disease, hypokalemia, hyperkalemia

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Contributor Information and Disclosures

Author

Steven J Compton, MD, FACC, FACP, Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals
Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society
Disclosure: Nothing to disclose.

Medical Editor

Justin D Pearlman, MD, PhD, ME, MA, Director of Advanced Cardiovascular Imaging, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center
Justin D Pearlman, MD, PhD, ME, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine
Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences
Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Reliant Grant/research funds Other; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD, Professor of Medicine and Pharmacology, Director, Clinical Cardiac Electrophysiology Fellowship Program, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center
Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)
Disclosure: Nothing to disclose.

 
 
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