Ventricular Tachycardia

Ventricular tachycardia (VT) refers to any rhythm faster than 100 beats per minute arising distal from the bundle of His. The rhythm may arise from working ventricular myocardium and/or the distal conduction system. VT may cause important symptoms such as syncope, palpitations, and dyspnea. With a few exceptions, VT is associated with increased risk of sudden death. The most common setting for VT is ischemic heart disease, in which myocardial scar is the substrate for electrical reentry. It is often, but not always, associated with hemodynamic compromise, particularly if the left ventricle is impaired or the heart rate is especially fast. When sustained VT causes signs or symptoms of diminished perfusion, emergent treatment is necessary.
VT is distinguished from ventricular fibrillation (VF), which is a grossly disorganized rapid ventricular rhythm that varies in both interval and waveform. VF may be difficult to distinguish from rapid polymorphic VT. Sudden death accounts for approximately half of all deaths from cardiovascular disease and is generally caused by VT and VF.
There is a slight overlap with accelerated idioventricular rhythm when an automatic VT is noted from 100-120 beats per minute.


Ventricular tachycardia (VT) is a general term that includes any rapid rhythm, faster than 100-120 beats per minute, arising in the ventricle. Regardless of the arrhythmia mechanism, the severity of clinical symptoms determines the urgency with which VT must be treated. During VT, cardiac output is reduced due to the rapid heart rate and lack of a properly timed or coordinated atrial contraction. Ischemia and mitral[1 ]insufficiency may also contribute to hemodynamic intolerance. Hemodynamic collapse is more likely when underlying left ventricular dysfunction is present or with very rapid rates. Diminished cardiac output may result in diminished myocardial perfusion, worsening inotropic response, and degeneration to VF, resulting in sudden death.

Monomorphic ventricular tachycardia

When the ventricular activation sequence is constant, the electrocardiographic pattern remains the same, and the rhythm is called monomorphic VT.
Monomorphic ventricular tachycardia.

Monomorphic ventricular tachycardia.

Monomorphic VT is most commonly seen in patients with underlying structural heart disease. There is typically a zone of slow conduction, most commonly due to scarring and/or fibrillar disarray. Causes include prior infarct, any primary cardiomyopathy, surgical scar, hypertrophy, and muscle degeneration. Reentrant tachycardias occur when an electrical wavefront travels slowly through the zone of slow conduction (usually damaged muscle protected by scar), allowing the rest of the circuit time to repolarize. The wavefront breaks out of the scar, activates the ventricle, and reenters the slow conduction zone. The QRS morphology during VT can be used to predict the exit site from the zone of slow conduction.[2 ]
Although most patients with VT have underlying structural heart abnormalities, monomorphic VT is occasionally observed in patients with structurally normal hearts. The clinical behavior of these VTs may be more consistent with triggered activity or abnormal automaticity. Monomorphic VTs are typically named for their site of origin. The most commonly involved sites are the RV outflow tract, LV outflow tract, LV septum, and the aortic root.[3 ]Although these arrhythmias have classically been considered benign, sudden death may occasionally be seen, despite the presence of a structurally normal heart.[4 ]

Polymorphic ventricular tachycardia

Polymorphic VT occurs when the ventricular activation sequence varies. It can be observed with or without structural heart disease. When polymorphic VT is observed in the setting of a prolonged resting QT electrocardiographic interval, it is termed torsade de pointes (torsades). Causes include certain drugs[5 ]and inherited defects in cardiac ion channel structure or expression. Most of the causative drugs block the delayed rectifier cardiac potassium current, IKr and include quinidine, erythromycin, haloperidol, and many others (see updated list).
Polymorphic ventricular tachycardia.

Polymorphic ventricular tachycardia.

Polymorphic VT and torsades are also observed in drug-free, structurally normal hearts when patients have genetic abnormalities affecting performance or intracellular processing of cardiac ion channels.[6,7 ]Examples include long QT syndrome, short QT syndrome,[8 ] Brugada syndrome,[9 ]idiopathic ventricular fibrillation, and familial catecholaminergic polymorphic VT.[10 ]
Inherited long QT syndrome is most commonly caused by mutations affecting the function or expression of the cardiac potassium channels IKr and IKs. Loss of channel activity results in delayed repolarization, measured as a prolonged QT interval on the electrocardiogram. Occasionally, disease is associated with errors in intracellular processing of the same channels. Interestingly, gain of function potassium channel mutations have been implicated in sudden death related to abnormally short QT intervals.[7 ]
Studies of other families with polymorphic VT have implicated the cardiac sodium channel (Brugada syndrome, some long QT syndromes), membrane calcium channels (Timothy syndrome), cardiac sarcoplasmic reticular calcium channels (familial adrenergic polymorphic VT, one form of arrhythmogenic right ventricular cardiomyopathy/dysplasia), and IK1 (Anderson-Tawil syndrome).
When polymorphic VT is observed in the absence of a cardiac channel defect, the most common causes are ischemia and myocarditis.


United States

The incidence of ventricular tachycardia (VT) in the United States is not well quantified because of the clinical overlap of VT with ventricular fibrillation (VF). Examination of sudden death data provides a rough estimate of VT incidence. Most sudden cardiac deaths are caused by VT or VF at an estimated rate of approximately 300,000 deaths per year in the United States, or about half of the estimated cardiac mortality in this country. A prospective surveillance study gave a sudden death incidence of 53 per 100,000, accounting for 5.6% of all mortality.[11 ]This is only a rough estimate of VT incidence because many patients have nonfatal VT and because arrhythmic sudden deaths may be associated with VF or bradycardia rather than VT.

The incidence of ventricular tachycardia (VT) in developed countries is thought to be similar to that of the United States. In other regions, VT incidence correlates with the prevalence of coronary artery disease.
Occasional pockets of unusual heart disease cause a locally increased risk of VT. Examples include the Greek island of Naxos (right ventricular dysplasia),[12 ]parts of South America (Chagas disease),[13 ]and northeastern Thailand (idiopathic VF).[14 ]

In patients with monomorphic ventricular tachycardia (VT), mortality risk correlates with the degree of structural heart disease. Underlying structural heart diseases, such as ischemic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, Chagas disease, and right ventricular dysplasia, have all been associated with monomorphic or polymorphic VT degenerating to ventricular fibrillation.
If VT is associated with hemodynamic collapse, morbidity in resuscitated survivors can include ischemic encephalopathy, acute renal insufficiency, transient ventricular dysfunction, aspiration pneumonitis, and trauma related to resuscitative efforts.
If VT is hemodynamically tolerated, the incessant tachyarrhythmia may also cause a dilated cardiomyopathy. This may develop over a period of several months and resolves with successful management of the VT.[15 ]A similar course is occasionally seen with ventricular bigeminy, despite the absence of sustained high rates.

Ventricular tachycardia risk within populations generally varies with the risk factors for atherosclerosis, rather than ethnic differences per se.
Certain genetic groups carry genetically mediated risk of unusual heart disease. Examples include the Veneto region of Italy and Greek island of Naxos (right ventricular dysplasia),[12 ] and northeastern Thailand (idiopathic ventricular fibrillation/Brugada syndrome)[14 ].

Ventricular tachycardia (VT) is observed more frequently in men because ischemic heart disease is more prevalent among men. Among patients with coronary artery disease in the Framingham study (see Framingham Heart Study), male deaths were more common than female deaths (46% vs 34%).[16 ]
Females with acquired or congenital long QT syndromes are at greater risk for sudden death. The opposite is true for arrhythmogenic right ventricular dysplasia (2-fold male predominance, and Brugada syndrome (~8-fold male predominance).

The incidence of ischemic ventricular tachycardia (VT) increases with age, regardless of sex, as the prevalence of coronary artery disease increases.
Among patients younger than 35 years, the most common causes of sudden death, and presumably of VT, include hypertrophic cardiomyopathy, right ventricular cardiomyopathy, myocarditis, and long QT syndrome. Idiopathic VT can be observed at any age.



Sustained ventricular tachycardia (VT) may precede a significant hemodynamic collapse. When this rhythm is present, it should be addressed rapidly.
  • The main symptoms of VT are palpitation, lightheadedness, and syncope from diminished cerebral perfusion. Chest pain may be due to ischemia or to the rhythm itself. Understandably, anxiety is often present. Syncope is more common in the setting of structural heart disease.
  • Some patients describe a sensation of neck fullness, which may be related to increased central venous pressure and cannon a waves. Cannon a waves are related to right atrial contraction against a closed tricuspid valve.
  • Dyspnea may be related to increased pulmonary venous pressures and occasional left atrial contraction against a closed mitral valve.
  • Risk factors include prior myocardial infarction, other known structural heart disease, or a family history of premature sudden death. VT must be strongly considered in any syncopal patient with such a history.
  • Any patient with a strong family history of premature (<40 y) sudden death should be evaluated for genetic arrhythmia syndromes, including long QT syndrome, short QT syndrome, Brugada syndrome, arrhythmogenic right ventricular dysplasia, and hypertrophic cardiomyopathy.

During ventricular tachycardia (VT)
  • Physical findings during VT include tachycardia, which is often associated with hypotension and tachypnea.
  • Signs of diminished perfusion may be present, including diminished level of consciousness, pallor, and diaphoresis.
  • Jugular venous pressure may be high, and cannon a waves may be observed if the atria are in sinus rhythm.
  • The first heart sound may vary in intensity due to loss of AV synchrony.
During sinus rhythm following conversion
  • Physical findings during normal rhythm are related to any underlying structural heart disease. These may include and may include displacement of the point of maximal impulse (PMI), murmurs related to valvular heart disease or hypertrophic cardiomyopathy, and an S3 gallop.
  • Rales may be present during sinus rhythm if uncompensated congestive heart failure is present.
  • Sinus rhythm is often interrupted by ventricular extrasystoles.

Coronary artery disease is the most common cause of ventricular tachycardia (VT).
  • Reentrant circuits may form and typically include the border zone between electrically inactive scar tissue and electrically active myocardial tissue. Paradoxically, the slower electrical conduction within such border zones predisposes to the development of fast reentrant arrhythmia circuits.
  • In developed countries, coronary artery disease is the most common cause of myocardial scar. The substrate for electrical reentry (VT) may occur with any process that creates myocardial scar tissue, including the dilated cardiomyopathies, hypertrophic cardiomyopathy, right ventricular dysplasia, Chagas disease, and surgical incisions in the ventricle.
  • As noted in the Pathophysiology section, VT is classified according to its electrocardiographic appearance.
Monomorphic ventricular tachycardia
  • When the same QRS electrocardiographic wave repeats itself, the VT is considered monomorphic. This implies a repetitive, identical activation sequence in the ventricle.
  • Monomorphic VT is most commonly due to repetitive activation of the same reentrant ventricular myocardial circuit.
  • Occasionally, monomorphic VT is related to repetitive automatic beats arising from the same ectopic focus.
Polymorphic ventricular tachycardia
  • When the QRS complex varies from beat to beat, the rhythm is described as polymorphic VT and suggests a variable electrical activation sequence. The most notorious, and probably the most common, form of polymorphic VT is torsade de pointes, a French term suggesting a "twisting of the points" of the QRS complexes over time. This term is now reserved for polymorphic VT observed in the setting of a prolonged QT interval. Other polymorphic VTs are occasionally observed during ischemia or myocarditis. 
    • Acquired QT prolongation is observed with certain potassium channel blocking medications. Most of the causative drugs block the delayed rectifier cardiac potassium current, IKr, and include quinidine, erythromycin, haloperidol, and many others. (See Drugs that Prolong the QT Interval and/or Induce Torsades de Pointes Ventricular Arrhythmia.)
    • Congenital long QT syndrome is a group of genetic disorders involving abnormal cardiac ion channels, (most commonly potassium channels responsible for ventricular repolarization).
    • In both acquired and congenital long QT syndromes, prolonged repolarization predisposes to torsade de pointes, which is most likely a reentrant rhythm with a constantly varying circuit. Other inherited ion channel abnormalities may cause idiopathic VF and familial polymorphic VT in the absence of QT prolongation.
  • In some patients, monomorphic VT occurs in the absence of structural heart disease (idiopathic VT).
    • These VTs are named according to their sites of origin, are often exercise dependent, and most often arise from the right and left ventricular outflow tracts and the left ventricular septum. The QRS morphology during tachycardia can be used to predict the VT site (see Images for examples).
    • Clinical behavior is generally consistent with an automatic, rather than reentrant, mechanism of origin. This becomes a critical point when treatment is considered. Although idiopathic VTs often respond to verapamil, this agent may cause hemodynamic collapse and death when administered to VT in patients with left ventricular dysfunction.
  • Triggers of VT include electrolyte abnormalities, ischemia, inflammation, and sleep apnea.
  • Hypokalemia is the most important arrhythmia trigger clinically, followed by hypomagnesemia. Hyperkalemia may also predispose to VT and VF, particularly in patients with structural heart disease.
  • Occasionally, VT is triggered by aggressive adrenergic stimulation, as is observed with cocaine use.

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


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 al[17 ]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
  • Vereckei et al refined a different algorithm based upon the single lead aVR.[18 ]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
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.

  • Diagnostic electrophysiologic study (EPS) requires placement of electrode catheters in the ventricle, followed by programmed ventricular stimulation using progressive pacing protocols. Premature ventricular beats[19 ]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.

EMERGENCY MANAGEMENT (click to enlarge)

Medical Care

Acute ventricular tachycardia
The acute emphasis is to achieve an accurate diagnosis and arrhythmia conversion. Ventricular tachycardia (VT) associated with loss of consciousness or hypotension is a medical emergency requiring immediate cardioversion. In a normal-sized adult, this is typically accomplished with a 100-to 200-J biphasic cardioversion shock using standard advanced cardiac life support (ACLS) protocols.
If the hemodynamic status is stable, and no evidence for coronary ischemia or infarction is present, then rhythm conversion may be achieved with either cardioversion or intravenous medication. An intravenous line is placed, and 12-lead ECG obtained prior to conversion. If left ventricular function is impaired, amiodarone, then lidocaine, are favored over procainamide because of the latter drug's potential for exacerbating congestive heart failure. If medical therapy is unsuccessful, synchronized cardioversion (50-200 J monophasic) following sedation is appropriate.
If runs of polymorphic VT are observed punctuated by sinus rhythm with QT prolongation, then attempts should be made to correct torsades with magnesium, isoproterenol, and/or pacing. Phenytoin and lidocaine may also help by shortening the QT interval in this setting, but procainamide is contraindicated because of its QT prolonging effects. Efforts should be made to correct hypokalemia and withdraw any chronic medications associated with QT-interval prolongation.
Occasionally, patients present with wide QRS complex tachycardia of unknown mechanism. In the absence of pacing, the differential diagnosis includes VT and aberrantly conducted supraventricular tachycardia (SVT). If hemodynamic compromise is present or if any doubt exists about the rhythm diagnosis, the safest strategy is to treat the undiagnosed rhythm as VT. If the clinical situation permits, a 12-lead ECG should be obtained prior to conversion of the rhythm. The ECG criteria of Brugada et al[17 ]may be useful in differentiating the arrhythmia mechanism as outlined above.
Rarely, patients present with repetitive runs of nonsustained VT, as in the following ECG. Prolonged exposure to this (or any other) tachycardia may cause a tachycardia-induced cardiomyopathy, which typically improves with medical or ablative therapy of the VT.[15 ]
Repetitive monomorphic ventricular tachycardia (V...
Repetitive monomorphic ventricular tachycardia (VT) from an asymptomatic 45-year-old female wind surfer with a structurally normal heart. This ECG pattern is typical for idiopathic VT arising from the right ventricular outflow tract.  This rhythm is often exertional and, unlike ischemic VT, suppressed by beta blockade or verapamil. The prognosis is good, with the following exceptions: (1) sudden death may be seen if right ventricular dysplasia or exceptionally rapid VT is encountered, and (2) occasionally, patients with incessant VT develop congestive heart failure due to tachycardia-induced cardiomyopathy or frequent ectopy. The cardiomyopathy resolves when the tachycardia is treated.
Ventricular tachycardia postconversion
Following conversion of VT, the clinical emphasis shifts to determining the severity of heart disease, prognosis, and best long-term management plan. Options, depending on the severity of symptoms and degree of structural heart disease, include medications, ICD implantation, and catheter ablation. Combinations of these therapies are often used when structural heart disease is present. Because monomorphic VT patients with structurally normal hearts have a low risk of sudden death, ICDs are rarely necessary in this setting. These patients are almost always managed with medications or ablation.
Antiarrhythmic drug trials have been disappointing, particularly in patients with left ventricular dysfunction. Some antiarrhythmic drugs may actually increase sudden death mortality in this group. This is of particular concern with Vaughn Williams Class I antiarrhythmics, which slow propagation and reduce tissue excitability through sodium channel blockade. Current clinical practice favors class III antiarrhythmics, which prolong myocardial repolarization through potassium channel blockade.
  • Amiodarone is a complex antiarrhythmic drug that deserves special mention. It is generally listed as a class III drug but has measurable class I, II, and IV effects. Unlike class I antiarrhythmics, amiodarone appears to be safe in patients with left ventricular dysfunction. Class III antiarrhythmics are preferred in most patients with left ventricular dysfunction.
  • In the setting of congestive heart failure, the best proven but nonspecific antiarrhythmic drug strategies include beta-receptor blocking drugs carvedilol, metoprolol, and bisoprolol; angiotensin-converting enzyme (ACE) inhibitors; and aldosterone antagonists. Statin therapy may also have nonspecific but salutory effects on both atrial and ventricular arrhythmias.
Surgical Care

In the 1980s, ventricular arrhythmia surgery was explored at several centers, using excision and cryoablation of infarct zones to prevent recurrent ventricular tachycardia (VT). This strategy has been essentially abandoned due to high mortality rates and the advent of both ICD and ablative therapies.
Implantable cardioverter-defibrillator
The implantable cardioverter-defibrillator (ICD) has changed the face of ventricular arrhythmia management. Like pacemakers, these devices can be implanted transvenously in a brief, low-risk procedure. Once installed, the ICD can detect ventricular tachyarrhythmias and terminate them with defibrillation shocks or antitachycardia pacing algorithms. These devices can also function as backup pacemakers in patients with bradyarrhythmias. The advent of transvenous ICD technology triggered several trials comparing the ICD to conventional antiarrhythmic therapies.
In patients with prior ventricular tachycardia/ventricular fibrillation, ICD therapy was compared with the best available antiarrhythmic drugs, amiodarone and sotalol. The Antiarrhythmics Versus Implantable Defibrillators (AVID) study; the Canadian Implantable Defibrillator Study (CIDS); and the Cardiac Arrest Study, Hamburg (CASH) demonstrated better survival in patients randomized to ICD therapy. The survival difference was significant in AVID, of borderline statistical significance in CIDS (P <0.06), and of no statistical difference in CASH. A meta-analysis of the 3 trials suggested a 28% reduction in the relative risk of death related to ICD implantation in this clinical setting.[20 ]
Endocardial catheter ablation
Endocardial catheter ablation is used early in idiopathic monomorphic VT (ie, structurally normal heart) but can also be used to reduce arrhythmia burden in the presence of cardiomyopathy. Ablation is used to treat symptomatic VT rather than to reduce sudden death risk. In patients with cardiomyopathy, the usual goal is to minimize the number of ICD shocks.
In some patients, percutaneous epicardial ablation can be used successfully when endocardial lesions fail. Current techniques include 3-dimensional scar, isopotential, or activation mapping, followed by high-energy radiofrequency ablation with irrigated-tip catheters capable of creating deeper lesions in the thicker LV wall.
  • Reentrant VT requires a slow conduction zone, and this is usually located along the border of a scarred zone of myocardium.
  • The small physical size of the slow conduction zone makes it an ideal target for focal ablation procedures.
  • Cell disruption can be achieved using radiofrequency energy or cryoablation via transvenous catheters during closed-chest procedures.
  • Because patients with ischemic VT often have multiple reentrant circuits, ablation is typically used as an adjunct to ICD therapy.
  • If VT arises from an automatic focus, the focus can be targeted for ablation.
  • In patients with structurally normal hearts, the most common form of VT arises from the right ventricular outflow tract (RVOT). The typical outflow tract ectopic beat shows a positive QRS axis in the inferior leads. Abnormal or triggered automaticity is the most likely mechanism, and focal ablation is curative in these patients. Ablation cure rates are typically greater than 95% if the arrhythmia can be induced in the electrophysiology laboratory.
  • Reentrant tachycardia may arise from the RVOT in patients with right ventricular dysplasia or repaired tetralogy of Fallot. These circuits are usually amenable to catheter ablation.

Cardiac electrophysiology is a subspecialty devoted to the diagnosis and management of cardiac arrhythmias. Patients with ventricular tachycardia should be referred to general cardiologists or electrophysiologists for specialized care.

Patients with ischemic ventricular tachycardia (VT) may benefit from low-cholesterol and/or low-salt diets. Patients with idiopathic VT may notice a reduction in symptoms when stimulants, such as caffeine, are avoided.

Ventricular tachycardia (VT) may be precipitated by increased sympathetic tone during strenuous physical exertion. One goal of successful VT management is to allow the patient to return to an active lifestyle through medications, ICD implantation, and/or ablation therapy.


Intravenous medications are used to suppress acute monomorphic ventricular tachycardia (VT). In the United States, these are limited to procainamide, lidocaine, amiodarone, and a handful of intravenous beta-adrenergic blocking agents (metoprolol, esmolol, propranolol). Bretylium is no longer available. In patients with cardiac arrest, intravenous amiodarone is the drug of choice. Although intravenous lidocaine is effective at suppressing peri-infarction VT, it may increase the overall mortality risk. Amiodarone has been shown to be superior to lidocaine or placebo in resuscitated cardiac arrest, but has not been as well studied in stable, monomorphic VT.
In patients with idiopathic VT (associated with structurally normal hearts), medications are often avoided entirely through the use of curative catheter-based ablation.
Oral medications are used to chronically suppress recurrent VT. As noted earlier in this article, current evidence favors class III antiarrhythmic drugs over class I drugs. No large studies compare the currently available class III drugs amiodarone and sotalol. Both drugs require careful monitoring during initiation and long term follow-up. Sotalol is loaded on an inpatient basis, with telemetry and ECG monitoring for bradycardia, ventricular proarrhythmia, and excessive QT prolongation. Many centers then follow sotalol patients on a quarterly basis to reassess renal function, QT intervals, and to watch for new drug interactions. Amiodarone initiation requires baseline and serial liver, thyroid, and pulmonary function testing.
When VT is observed in a patient receiving an antiarrhythmic drug, discrimination must be made between VT recurrence and drug-induced ventricular proarrhythmia. The most common form of proarrhythmia is torsades de pointes (see Torsade de Pointes) associated with QT-interval prolongation, usually due to excessive potassium channel blockade.
In patients with hemodynamically significant VT/VF, implantable cardioverter-defibrillator (ICD) implantation has superseded medication as primary therapy. Because ICDs treat, rather than prevent, ventricular arrhythmias, as many as 50% of ICD patients require therapy with antiarrhythmic drugs to reduce the potential for ICD shocks. Once an ICD has been implanted, adjunctive drug and catheter ablation therapies can be used to reduce the number of ICD discharges.
Intravenous administration is used for suppression of acute VT. Agents alter the electrophysiologic mechanisms responsible for arrhythmia. Medications are generally used to prevent recurrence of VT in susceptible patients.
Careful attention must be paid to drug pharmacokinetics due to relatively narrow therapeutic windows involved.
Most antiarrhythmic drugs may actually cause ventricular arrhythmias, and risks generally increase with serum drug levels.
To monitor for drug proarrhythmia, patients are usually admitted to the hospital during initiation of oral antiarrhythmic medication.  The patient is then monitored by telemetry and serial ECGs during 5-6 drug half-lives to be sure that the drug is well tolerated.
Lidocaine (Xylocaine, Nervocaine, LidoPen, Duo-Trach)
Class IB antiarrhythmic that increases electrical stimulation threshold of the ventricle, suppressing automaticity of conduction through the tissue. Although lidocaine may terminate VT successfully, it may increase the overall mortality in peri-infarction VT. Evidence for effectiveness is considered "Indeterminate" in the 2000 American Heart Association Emergency Cardiovascular Care guidelines.
1-1.5 mg/kg IV push, followed by 0.5-0.75 mg/kg IV push to a maximum of 3 mg/kg
Continuous 1–4 mg/min infusion should be started after arrhythmia is suppressed
Endotracheal, intraosseous, and IV loading dose: 1 mg/kg, may repeat twice at 10- to 15-min intervals if necessary; follow with continuous IV infusion of 20-50 mcg/kg/min
Coadministration with cimetidine or beta-blockers, increases toxicity of lidocaine; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine
Documented hypersensitivity to amide-type local anesthetics; avoid in Adams-Stokes syndrome and Wolf-Parkinson-White syndrome; avoid in severe sinoatrial, atrioventricular (AV), or intraventricular block if artificial pacemaker not in place
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Do not use a drug solution that contains preservatives; caution in heart failure, hepatic disease, hypoxia, hypovolemia or shock, respiratory-depression, and bradycardia; elderly patients may be at increased risk for CNS and cardiac adverse effects due to increased half-life or decreased clearance of the drug; high plasma concentrations can cause seizures, heart block, and AV conduction abnormalities; has been associated with malignant hyperthermia
Procainamide (Procanbid, Pronestyl)
A Class IIB level therapy used for VT refractory to defibrillation and epinephrine. Increases refractory period of atria and ventricles.
Myocardial excitability is reduced by increase in threshold for excitation and inhibition of ectopic pacemaker activity.
20-30 mg/min continuous IV infusion until arrhythmia suppressed, patient becomes hypotensive, QRS widens 50% above baseline, or maximum dose of 17 mg/kg is administered; once arrhythmia is suppressed, may be infused at rate of 1-4 mg/min continuously
Long-acting formulation: 1000 mg PO bid; adjust dose based on levels of procainamide and NAPA
Not established; suggested dosage is 15-50 mg/kg/d PO divided q3-6h to maximum 4 g/d
Alternatively, 20-30 mg/kg/d IM divided q4-6h to maximum 4 g/d or 3-6 mg/kg per dose IV infused over 5 min
Maintenance: 20-80 mcg/kg/min IV by continuous infusion; not to exceed 100 mcg per dose or 2 g/d
Can expect increased levels of procainamide metabolite NAPA in patients taking cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim, and quinidine; procainamide may increase effect of skeletal muscle relaxants, quinidine, lidocaine, and neuromuscular blockers; ofloxacin inhibits tubular secretion of procainamide and may increase bioavailability; when taken concurrently with sparfloxacin, may increase risk of cardiotoxicity
Complete heart block or second- or third-degree heart block, if pacemaker not in place; torsade de pointes; documented hypersensitivity; systemic lupus erythematosus
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Monitor for hypotension; plasma concentrations of procainamide and active metabolite, NAPA, may increase in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; caution in complete AV block, digitalis intoxication, organic heart disease, renal disease, and hepatic insufficiency
Amiodarone (Cordarone, Pacerone)
Now the drug of choice in treatment of unstable ventricular arrhythmias. Currently considered a Class IIb intervention by the American Heart Association 2000 Emergency Cardiovascular Care Guidelines. Prehospital studies currently suggest that amiodarone is safe and efficacious for use in out-of-hospital cardiac arrest. Often used for life-threatening ventricular arrhythmias in patients who have relative contraindications to its use.
150 mg IV infused over 10 min, follow with 1 mg/min constant infusion for 6 h, then maintenance infusion at 0.5 mg/min
Oral dosing generally 400 mg/d following load
Not established; weight-based dosing suggested; consider for refractory ventricular arrhythmias in children
Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity of amiodarone is increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause an additive effect and decrease myocardial contractility further; cimetidine may increase amiodarone levels
Documented hypersensitivity; sinus node dysfunction; atrioventricular conduction disorders; underlying hepatic, pulmonary, or thyroid disease
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Hypotension, bradycardia, and AV block may occur; hypotension is most common adverse effect during intravenous administration; acute life-threatening pulmonary or hepatic toxicity may complicate acute or chronic use of this drug; elevation of serum hepatic enzymes and/or TSH requires that patients be monitored carefully during amiodarone therapy; rarely, irreversible blindness from optic neuritis is observed with chronic use
Sotalol (Betapace)
Primarily a potassium channel (IKr)–blocking drug, with weak beta-blocker effect. In ESVEM study, sotalol was compared with 6 other drugs (not including amiodarone) in VT patients.
Survival was best in the sotalol group.
80-120 mg PO q12h initially; occasionally, doses as high as 240 mg q12h are used with careful monitoring for toxicity


Further Inpatient Care

  • Initiation of antiarrhythmic medications may require telemetry monitoring for drug-induced proarrhythmia. Monitor patients starting class Ia drugs and class III drugs for QTc prolongation and torsade de pointes until steady-state drug levels (5 or more clearance half-lives) have been reached. A notable exception is amiodarone administration, which may require months to achieve steady state. Drug loading of amiodarone necessarily is completed on an outpatient basis.
  • Class Ic antiarrhythmics are associated with drug-induced ventricular tachycardia and rate-related conduction slowing. Many centers commit their patients to telemetry monitoring and predischarge exercise testing during initiation of Ic agents. Sinus bradycardia and sinus node dysfunction are often exacerbated by antiarrhythmic drugs.
  • The possibility of drug-specific noncardiac adverse effects requires special vigilance. These effects are drug-specific (visual disturbances with flecainide, joint pains with procainamide) and emphasize the need for physicians to be familiar with these medications.
Further Outpatient Care

  • Patients receiving chronic antiarrhythmic therapy should be observed regularly for proarrhythmia and adverse effects. Adverse reactions may be observed at any time during the course of drug therapy. The risk of amiodarone-induced liver, lung, thyroid, and other toxicities has prompted publication of specific follow-up guidelines.[21 ]
  • Chronic procainamide administration may be associated with a lupus syndrome. Life-threatening pulmonary and hepatic toxicities are well known in patients receiving amiodarone.
  • Patients should be questioned carefully about recurrent palpitations and syncope.
  • Patients with implantable cardioverter-defibrillators (ICDs) require regular outpatient device follow-up to allow monitoring of battery and transvenous lead status. Although the battery lifetime is somewhat predictable, lead fracture and failure may occur at any time. In addition, efficacy of the device should be rechecked following initiation of medications that may increase the ventricular defibrillation threshold. This is typically accomplished with an outpatient noninvasive programmed stimulation study (NIPS) carried out through the implanted device.
  • Lead problems can generally be diagnosed in clinic and occasionally require lead revision or replacement.
Inpatient & Outpatient Medications

  • Because most patients with ventricular tachycardia have an underlying cardiomyopathy, continued therapy of congestive heart failure and coronary artery disease remains important.
  • Outpatient medication choices depend upon the degree of ventricular dysfunction, comorbid disease such as asthma, and the presence or absence of an implantable cardioverter-defibrillator.

Prognosis varies with the specific cardiac process but is predicted best by left ventricular function. In patients with ischemic cardiomyopathy and nonsustained ventricular tachycardia (VT), sudden death mortality rates approach 30% in 2 years. In patients with idiopathic VT, the prognosis is excellent and the major risk is due to poorly timed syncopal spells. A few exceptions exist to the above rule. Patients with long QT syndrome, right ventricular dysplasia, and hypertrophic cardiomyopathy may be at increased risk of sudden death despite relatively preserved left ventricular function. These possibilities should be considered in any patient with a strong family history of premature sudden death.
Patient Education

For excellent patient education resources, visit eMedicine's Heart Center, Cholesterol Center, and Public Health Center. Also, see eMedicine's patient education articles Heart Rhythm Disorders, Coronary Heart Disease, Chest Pain, Heart Attack, Cardiopulmonary Resuscitation (CPR), Supraventricular Tachycardia, and Palpitations.


Medicolegal Pitfalls

  • Confusion with supraventricular tachycardia (SVT)
    • Occasionally, patients present with hemodynamically stable ventricular tachycardia (VT).
    • Hemodynamic stability does not help discriminate VT from SVT.
    • Hemodynamic deterioration and death have been reported from inappropriate use of verapamil in this setting.
  • Confusion with paced rhythms
    • Occasionally, patients present with rapid rhythms generated by permanent pacemakers. The most common cause is tracking of atrial tachyarrhythmias, such as atrial flutter or fibrillation. The pacemaker typically paces around the programmed maximum tracking limit, which is often set at 120-140 beats per minute in older patients.
    • If a pacemaker programmer is not available, a magnet placed over the pacer generator deactivates atrial sensing temporarily and allows diagnosis of the atrial arrhythmia.
  • Missed diagnoses
  • Patients with sudden death may present with syncope first.
  • In a syncopal patient, the ECG should be screened carefully for myocardial infarction, conduction abnormalities, QT-interval prolongation, precordial T-wave inversions, ventricular preexcitation, and ventricular hypertrophy.
  • Patients treated chronically with antiarrhythmic drugs require careful follow-up to minimize the risk of proarrhythmia and other adverse effects.

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