Stanford Cardiac Arrhythmia Service

Ventricular Tachycardia (VT)

Ventricular tachycardia is a rapid heart rhythm occurring from the ventricles, the main pumping function.  The rates are most commonly 150 to 250 beats per minute but ventricular tachycardia may occur at relatively slow rates such as 110 to 150 beats per minute, sometimes due to medications that slow the ventricular tachycardia or advanced degrees of heart impairment. 

Ventricular tachycardia may be so rapid that they prevent the heart from effectively beating or pumping blood to the entire body. This results in loss of blood flow to the vital organs including the brain, leading to loss of consciousness. 

Ventricular tachycardia is a rapid heart rhythm occurring from the ventricles, the main pumping function.  The rates are most commonly 150 to 250 beats per minute but ventricular tachycardia may occur at  relatively slow rates such as 110 to 150 beats per minute, sometimes due to medications that slow the ventricular tachycardia or advanced degrees of heart impairment. 



Although most patients with VT have structural heart disease, usually with prior myocardial infarction or cardiomyopathy, impairment of the heart pumping function, there are several subsets of patients without any structural heart abnormalities.
These forms of ventricular tachycardia fall into several categories:
Right ventricular and left ventricular outflow tract tachycardias
Fascicular tachycardias

Of the outflow tract tachycardias, the right ventricular outflow tract tachycardias (RVOT) are the most common.  These tachycardias have a typical characteristic ECG appearance with a left bundle branch block appearance and are positive in the inferior leads of the ECG. Typically the onset of R wave is at V4.

The RVOT tachycardias are generally considered benign. They may result in recurrent symptoms of palpitations and dizziness and less commonly loss of consciousness.  There are limited data suggesting that a small subset of patients with RVOT tachycardias that are extremely rapid or result in loss of consciousness may have a greater risk associated with them but these data are inconclusive.  Overall, the RVOT tachycardias are not considered life-threatening. 

The RVOT tachycardias are commonly triggered by sympathetic stimulation such as anxiety and excitement. In additional stimulants such as caffeine seem to have a provocative role.  In pre-menopausal women, hormonal influences also seem to be significant.

The initial evaluation of patients with suspected normal heart ventricular tachycardias centers around confirming that there are no subtle abnormalities of the heart, particularly the right ventricle.  Echocardiography is usually the first step with some patients also receiving a cardiac MRI with delayed enhancement.   This is particularly important to exclude mild forms of arrhythmogenic right ventricular dysplasia/cardiomyopathy. 

Patients with a family history of sudden death and apparent RVOT tachycardia should be particularly thoroughly with a cardiac MRI.

The next step in the evaluation is the documentation of the ECG pattern of the ventricular tachycardia on an ECG with all 12 leads.  This documentation is necessary to confirm that the pattern is consistent RVOT tachycardia.  If the ECG pattern is atypical, for example, one might be more concerned about mild forms of arrhythmogenic right ventricular dysplasia/cardiomyopathy. 

The treatment of RVOT tachycardias begins with reassurance since understanding that although this is a form of ventricular tachycardia, the condition is felt to be benign.  The next step is avoidance of any stimulants such as caffeine that may be exacerbating the arrhythmias.  Pharmacologic therapy usually starts with beta-blocker therapy.  Beta-blocker therapy is usually more effective than calcium channel blocker therapy.  If the patient remains particularly symptomatic despite pharmacologic therapy, one may consider catheter ablation of the RVOT tachycardia.  Patients with frequent PVCs (for example 5-10%) provide an excellent endpoint in addition to the inability to produce the PVCs with isoproterenol, an adrenalinelike substance.   This therapeutic approach is the same for patients with highly symptomatic PVCs without ventricular tachycardia if the PVCs are localized to the RVOT.  The threshold for PVC or RVOT ablation is relatively low if there are frequent PVCs since because the ablation does not require access to the left side of the heart which has a higher risk of stroke and other complications and the success is generally high. 

Less commonly than RVOT tachycardias there are tachycardias that arise from the left ventricular outflow tract and the aortic cusp region.  These tachycardias may have a very different ECG appearance from RVOT but some left outflow tract tachycardias have more subtle differences for example with earlier R wave transition in the precordium of V2-V3.  The pharmacologic responsiveness is generally similar to that of RVOT tachycardias.  The threshold for catheter ablation however is generally felt to be higher because of increased risk: left sided access is associated with higher risk of stroke, the coronary artery origins are located near the coronary cusps, the aorta may be mechanically damaged, and the conduction system may be nearby. 

The next most common site for patients with normal heart ventricular tachycardias is the region of the fascicles, a part of the conduction system that carries the electrical signals to the left side of the heart.  These tachycardias are typically of a right bundle branch block pattern.

3-dimensional mapping may be used to determine the site of the tachycardia extremely accurately.

There are miscellaneous other ventricular tachycardias that are not included in the categories above.

Ventricular tachycardia in the setting of cardiomyopathy are the most common forms of ventricular tachycardia.  In patients with prior myocardial infarction, the patients are felt to have ischemic cardiomyopathy.  The myocardial infarction may have a central area of scar surrounded by islands of scar interspersed with living tissue. These channels of living tissue are felt to be the pathways or corridors for electrical signals to travel.  Most ventricular tachycardias in the setting of cardiomyopathy are felt to be reentrant, meaning that they take a roughly circular path over and over again.


Patients with cardiomyopathy and ventricular tachycardia are treated with an implantable defibrillator because of the risk of sudden cardiac death.  Patients with ischemic and nonischemic cardiomyopathy may have a variable frequency of recurrent ventricular tachycardia.  Patients with multiple VT shocks are typically good candidates for ventricular tachycardia ablation.  Generally the patients are ambulatory without advanced and progressive heart failure. 

In ischemic cardiomyopathy, most VT circuits are located close to the inner surface of the heart, the endocardium and therefore may be approached with catheters endocardially.   In most situations, the artery in the groin the femoral artery is accessed and a catheter is advanced to the aorta and then across the aortic valve into the left ventricle.  The alternative is to access the femoral vein and puncture across the atrial septum called a transseptal catheterization and enter the left ventricle in that manner.

The process of VT ablation begins with performing a map by making recordings at over 100 sites in the left ventricle.  This map will define the nature of the endocardial scar and the islands of living tissue.

Major advances in catheter ablation have resulted in dramatic improvements in the results of VT ablation. VT ablation targets the regions of VT circuit such as slow conduction zones called the isthmus.  3-dimensional mapping systems permit identification of the critical parts of the circuit without inducing VT, a technique called substrate mapping.  Ablating VT without the need to induce VT increases safety and success of the procedure.
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VT ablation results in most patients in a significant reduction in the number of VT episodes.

In patients with nonischemic cardiomyopathy, the likelihood of there being significant scar on the epicardial surface increases significantly.  In such patients if endocardial mapping and ablation, epicardial access is necessary. In patients without prior cardiac surgery it is possible to obtain access to the space outside the heart, called the pericardial space to perform the mapping and ablation.

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