Ventricular Tachycardia Treatment & Management

Updated: Dec 31, 2015
  • Author: Steven J Compton, MD, FACC, FACP, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
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Treatment

Approach Considerations

Sustained ventricular tachycardia (VT) may lead to hemodynamic collapse. Consequently, these patients require urgent conversion to sinus rhythm. The strategy for conversion depends on whether the patient is hemodynamically stable or unstable.

Unstable patients have signs or symptoms of insufficient oxygen delivery to vital organs as a result of the tachycardia. Such manifestations may include the following:

  • Chest pain
  • Dyspnea
  • Hypotension
  • Altered level of consciousness

In the workup, this situation must be differentiated from clinical manifestations of an underlying medical condition that is causing secondary tachycardia.

Unstable patients with monomorphic VT should be immediately treated with synchronized direct current (DC) cardioversion, usually at a starting energy dose of 100 J (monophasic; comparable biphasic recommendations are not currently available). Unstable polymorphic VT is treated with immediate defibrillation. The defibrillator may have difficulty recognizing the varying QRS complexes; therefore, synchronization of shocks may not occur.

Stable patients have adequate vital end-organ perfusion and thus do not experience signs or symptoms of hemodynamic compromise. Treatment depends on whether the VT is monomorphic or polymorphic and whether left ventricular function is normal or impaired (eg, reduced left ventricular ejection fraction [LVEF] or heart failure).

In stable patients with monomorphic VT and normal left ventricular function, restoration of sinus rhythm is typically achieved with intravenous (IV) procainamide or sotalol. Lidocaine may also be used. A 12-lead electrocardiogram (ECG) is obtained before conversion.

If left ventricular function is impaired, amiodarone (or lidocaine) is preferred to procainamide for pharmacologic conversion because of the latter drug’s potential for exacerbating heart failure. However, mounting evidence indicates that amiodarone should not be the first-line antiarrhythmic for stable VT, because its effects on myocardial conduction and refractoriness are gradual in onset. [35, 36, 37, 38] If medical therapy is unsuccessful, synchronized cardioversion (50-200 J monophasic) following sedation is appropriate.

Polymorphic VT in stable patients typically terminates on its own. However, it tends to recur. After sinus rhythm returns, the ECG should be analyzed to determine whether the QT interval is normal or prolonged. Polymorphic VT in patients with a normal QT interval is treated in the same manner as monomorphic VT.

If the patient has runs of polymorphic VT punctuated by sinus rhythm with QT prolongation, treatment is with magnesium sulfate, isoproterenol, pacing, or a combination thereof. Phenytoin and lidocaine may also help by shortening the QT interval in this setting, but procainamide and amiodarone are contraindicated because of their QT-prolonging effects. Magnesium is unlikely to be effective in patients with a normal QT interval. [25]

In patients with electrolyte imbalances (eg, hypokalemia or hypomagnesemia from diuretic use), correction of the abnormality may be necessary for successful cardioversion. In patients with severe digitalis toxicity (eg, with sustained ventricular arrhythmias, advanced atrioventricular [AV] block, or asystole), treatment with antidigitalis antibody may be indicated. [25]

After conversion of VT, the clinical emphasis shifts to determining the severity of heart disease, assessing the prognosis, and formulating the best long-term management plan. Options, depending on the severity of symptoms and degree of structural heart disease, include the following:

Combinations of these therapies are often used when structural heart disease is present.

Antiarrhythmic drugs have traditionally been the mainstays of treatment for clinically stable patients with VT. However, some patients experience unacceptable side effects or frequent recurrence of VT with drug therapy. As a result, cardiologists are increasingly making use of devices and procedures designed to abort VT or to remove the dysrhythmogenic foci in the heart. In patients with idiopathic VT (associated with structurally normal hearts), medications are often avoided entirely through the use of curative catheter-based ablation.

Congenital long QT syndrome and catecholamine polymorphic VT have been linked to sudden cardiac death. Patients with these disorders are managed with a combination of genetic typing, beta blockers, lifestyle modification, and, in selected cases, ICD placement. [40]

In the 1980s, several centers explored ventricular arrhythmia surgery, using excision and cryoablation of infarct zones to prevent recurrent VT. This strategy has been essentially abandoned as a consequence of the high mortality and the advent of ICDs and ablative therapies.

Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death have been developed jointly by the American College of Cardiology (ACC), the American Heart Association (AHA), and the European Society of Cardiology (ESC). [25]

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Initial Supportive Management

Rapid transport to an emergency department (ED) is essential. Emergency medical service (EMS) personnel may be called upon to provide cardioversion/defibrillation in the field if they have sufficient training and if appropriate protocols exist.

EMS personnel must pay adequate attention to the primary survey and address airway, breathing, and circulation as necessary. Beyond those steps, vascular access, supplemental oxygen, and ECG rhythm strip monitoring are all-important but should not delay rapid transport to the ED for definitive care.

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Cardioversion in Acute Ventricular Tachycardia

The acute emphasis in patients with VT is on achieving an accurate diagnosis and conversion to sinus rhythm. VT associated with loss of consciousness or hypotension is a medical emergency necessitating immediate cardioversion. In a normal-sized adult, this is typically accomplished with a 100- to 200-J biphasic cardioversion shock administered according to standard Advanced Cardiovascular Life Support (ACLS) protocols. [41, 42]

Reversible risk factors for VT should be addressed. Efforts should be made to correct hypokalemia and to withdraw any long-term medications associated with QT-interval prolongation.

When VT occurs in patients with ongoing myocardial ischemia, lidocaine is suggested as the primary antiarrhythmic medication, because the mechanism in these cases is thought to be abnormal automaticity rather than reentry. [43] Although IV lidocaine is effective at suppressing peri-infarction VT, it may increase the overall mortality risk. In situations involving torsades de pointes, magnesium sulfate may be effective if a long QT interval is present at baseline.

Synchronized cardioversion should be considered at an early stage if medical therapy fails to stabilize the rhythm. The initial shock energy should be 100 J (monophasic), followed by higher shock energies if the response is inadequate.

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; see the images below). If hemodynamic compromise is present or if any doubt exists about the rhythm diagnosis, the safest strategy is to treat the rhythm as VT.

Supraventricular tachycardia with aberrancy. Traci Supraventricular tachycardia with aberrancy. Tracing is from patient with structurally normal heart who has normal resting ECG. This rhythm is orthodromic reciprocating tachycardia with rate-related left bundle-branch block. Note relatively narrow RS intervals in precordial leads.
ECG from 48-year-old man with wide-complex tachyca ECG from 48-year-old man with wide-complex tachycardia during treadmill stress test. Any wide-complex tachycardia tracing should raise possibility of ventricular tachycardia, but closer scrutiny confirms left bundle-branch block conduction of supraventricular rhythm. By Brugada criteria, RS complexes are apparent in precordium (V2-V4), and interval from R wave onset to deepest part of S wave is < 100 ms in each of these leads. Ventriculoatrial dissociation is not seen. Vereckei criteria are based solely upon aVR, which shows no R wave, initial q wave width < 40 ms, and no initial notching in q wave. Last Vereckei criterion examines slope of initial 40 ms of QRS versus terminal 40 ms of QRS complex in aVR. In this case, initial downward deflection in aVR is steeper than terminal upward deflection, yielding Vi/Vt ratio >1. All of these criteria are consistent with aberrantly conducted supraventricular tachycardia. Gradual rate changes during this patient's treadmill study (not shown here) were consistent with sinus tachycardia mechanism.

If the clinical situation permits, a 12-lead ECG should be obtained before conversion of the rhythm. The ECG criteria of Brugada et al [4] may be useful in differentiating the arrhythmia mechanism (see Workup).

Rarely, patients present with repetitive runs of nonsustained VT. Prolonged exposure to this (or any other) tachycardia may cause a tachycardia-induced cardiomyopathy, which typically improves with medical or ablative treatment of the VT. [8]

Pulseless VT

Pulseless VT, in contrast to other unstable VT rhythms, is treated with immediate defibrillation. High-dose unsynchronized energy should be used. The initial shock dose on a biphasic defibrillator is 150-200 J, followed by an equal or higher shock dose for subsequent shocks. If a monophasic defibrillator is used, the initial and subsequent shock dose should be 360 J.

Shock administration should be followed by immediate chest compressions, airway management with supplemental oxygen, and vascular access with administration of vasopressors. In cases of shock-resistant pulseless VT, the use of antiarrhythmic medications may be considered. IV amiodarone is the drug of choice.

Vasopressors can include epinephrine 1 mg IV given every 3-5 minutes or, in lieu of epinephrine, vasopressin 40 units IV as a 1-time dose. [44] ACLS drug-therapy guidelines recommend the use of IV amiodarone or lidocaine as the first-line adjunctive antiarrhythmic treatment of shock-resistant pulseless VT. [45, 46]

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Poststabilization Management

After initial treatment and stabilization, patients with VT generally should undergo the following:

  • Referral to a cardiologist
  • Admission to a monitored bed
  • Further studies, such as electrophysiologic study (EPS)
  • Consideration for radiofrequency ablation (RFA)
  • Consideration for ICD placement

Initiation of antiarrhythmic medications may require telemetry monitoring for drug-induced proarrhythmia. Patients starting class IA and class III drugs should be monitored for corrected QT (QTc) prolongation and torsades de pointes until steady-state drug levels (≥5 clearance half-lives) have been reached. A notable exception is amiodarone, which may require months to achieve steady state; drug loading of amiodarone necessarily is completed on an outpatient basis. [47]

Class IC antiarrhythmics are associated with drug-induced VT and rate-related conduction slowing. Many centers commit their patients to telemetry monitoring and predischarge exercise testing during initiation of agents from this class. Sinus bradycardia and sinus node dysfunction are often exacerbated by antiarrhythmic drugs.

In adult patients with ventricular arrhythmias whose age, gender, and symptoms indicate a moderate or greater likelihood of coronary heart disease, the ACC/AHA/ESC guidelines recommend exercise testing to provoke ischemic changes or ventricular arrhythmias. [25] Regardless of age, exercise testing is useful in patients with established or suspected exercise-induced ventricular arrhythmias, including catecholaminergic VT, to provoke the arrhythmia, to confirm a diagnosis, and to ascertain the patient’s response to tachycardia. [25]

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Long-Term Treatment

Patients with monomorphic VT who have structurally normal hearts are at a low risk of sudden death. Consequently, 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 a particular concern with Vaughan Williams class I antiarrhythmics, which slow propagation and reduce tissue excitability through sodium-channel blockade. For most patients with left ventricular dysfunction, current clinical practice favors class III antiarrhythmics, which prolong myocardial repolarization through potassium-channel blockade. [48]

Amiodarone is a complex antiarrhythmic drug that deserves special mention. It is generally listed as a class III agent but has measurable class I, II, and IV effects. Unlike class I antiarrhythmics, amiodarone appears to be safe in patients with left ventricular dysfunction.

As per the ACC/AHA/ESC 2006 guidelines, amiodarone, when used in combination with beta blockers, can be useful for patients with left ventricular dysfunction due to previous myocardial infarction (MI) and symptoms due to VT that do not respond to beta blockers. [25]

In the Electrophysiologic Study versus Electrocardiographic Monitoring (ESVEM) trial, which compared long-term treatment with 7 antiarrhythmic drugs (not including amiodarone) in patients with VT, the risks of adverse drug effects, arrhythmia recurrence, or death from any cause were lowest with sotalol. [48] The other antiarrhythmic drugs studied in the ESVEM trial were imipramine, mexiletine, pirmenol, procainamide, propafenone, and quinidine.

In patients with heart failure, the best-proven—albeit nonspecific—antiarrhythmic drug strategies include the use of the following:

  • The beta receptor–blocking drugs carvedilol, metoprolol, and bisoprolol
  • Angiotensin-converting enzyme (ACE) inhibitors
  • Aldosterone antagonists

According to the ACC/AHA/ESC guidelines, statin therapy is advantageous in patients with coronary heart disease, to reduce the risk of vascular accidents, ventricular arrhythmias (possibly), and sudden cardiac death. [25]

Although idiopathic VTs often respond to verapamil, this agent may cause hemodynamic collapse and death when administered to treat VT in patients with left ventricular dysfunction. Therefore, verapamil (or any other calcium-channel blockers) is contraindicated in any patient with wide-complex tachycardia of uncertain etiology. [37]

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Catheter Ablation

RFA via endocardial or epicardial catheter placement can be used to treat VT in patients with left ventricular dysfunction from previous MI, [49] cardiomyopathy, bundle-branch reentry, and various forms of idiopathic VT (see the image below). [25]

Curative ablation of ventricular tachycardia (VT). Curative ablation of ventricular tachycardia (VT). Patient had VT in setting of ischemic cardiomyopathy. VT was induced in electrophysiology laboratory, and ablation catheter was placed at critical zone of slow conduction within VT circuit. Radiofrequency (RF) energy was applied to tissue through catheter tip, and VT terminated when critical conducting tissue was destroyed.

Current techniques include 3-dimensional scar, late potential, and activation mapping, followed by high-energy RFA with irrigated-tip catheters capable of creating deeper lesions in the thicker left ventricular wall. In some patients, percutaneous epicardial ablation can be used successfully when endocardial lesions fail. [50, 51]

Catheter ablation is used early in patients with idiopathic monomorphic VT (ie, VT in a structurally normal heart arising from a focal source) that is resistant to drug therapy, as well as in those who are drug-intolerant or do not wish to have long-term drug therapy. [25] In these patients, ablation is used to treat symptoms rather than to reduce the risk of sudden death. In patients with structurally normal hearts, Catheter ablation can eliminate symptomatic VT arising from the right or left ventricle.

Catheter ablation may also be used in patients with cardiomyopathy. The goal in these cases is to reduce arrhythmia burden and thereby minimize the number of ICD shocks.

The ACC/AHA/ESC guidelines recommend ablation in patients with bundle-branch reentrant VT. [25] Most ischemic reentrant VT requires a slow conduction zone, which 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 by using RFA or cryoablation via transvenous catheters during closed-chest procedures.

In a study of 2061 patients with scar-related VT, Tung et al found that patients who experience no VT recurrence after catheter ablation have an increased rate of transplant-free survival. The investigators determined that following ablation, 70% of the study’s patients, who suffered from ischemic or nonischemic cardiomyopathy, were free from VT recurrence for a year, with cardiac transplantation-free survival being 90% at 1 year in those without VT recurrence, compared with 71% in patients with recurrence. [52]

A 2-center study examined the use of a percutaneous left ventricular assist device (pLVAD) in patients undergoing ablation for scar-related VT. [53] Use of a pLVAD allowed maintenance in VT for a significantly longer period by virtue of its ability to maintain end-organ perfusion. Whether this effect will translate into clinical benefits is unclear. At the least, however, this study demonstrates the benefit of pLVADs in patients with scar-related unstable VT.

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 typically exceed 95% if the arrhythmia can be induced in the electrophysiology laboratory. Difficulty of outflow tract ablation may be predicted by ECG morphology. [54]

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 (see the image below). [55]

Posteroanterior view of right ventricular endocard Posteroanterior view of right ventricular endocardial activation map during ventricular tachycardia in patient with prior septal myocardial infarction. Earliest activation is recorded in red, late activation as blue to magenta. Fragmented low-amplitude diastolic local electrograms were recorded adjacent to earliest (red) breakout area, and local ablation in this scarred zone (red dots) resulted in termination and noninducibility of this previously incessant arrhythmia.

Bohnen et al performed a prospective study to assess the incidence and predictors of major complications from contemporary catheter ablation procedures. [56] Major complication rates ranged from 0.8% (SVT) to 6% (VT associated with structural heart disease), depending on the ablation procedure performed. These researchers reported that renal insufficiency was the only independent predictor of a major complication. [56]

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Implantable Cardioverter-Defibrillator Placement

The ICD has changed the face of ventricular arrhythmia management. Like pacemakers, these devices can be implanted transvenously in a brief, low-risk procedure. Once implanted, the ICD can detect ventricular tachyarrhythmias and terminate them with defibrillation shocks or antitachycardia pacing algorithms (see the image below).

Termination of ventricular tachycardia (VT) with o Termination of ventricular tachycardia (VT) with overdrive pacing. Patient has reentrant VT, which is terminated automatically by pacing from implantable cardioverter-defibrillator.

Newer guidelines recommend ICD therapy to augment medical management for the following [1] :

  • Most patients with hemodynamically unstable VT
  • Most patients with prior MI and hemodynamically stable sustained VT
  • Most cardiomyopathy patients with unexplained syncope
  • Most patients with genetic sudden death syndromes when unexplained syncope is noted

In patients with prior VT or ventricular fibrillation (VF), the Antiarrhythmics Versus Implantable Defibrillators (AVID) study, the Canadian Implantable Defibrillator Study (CIDS), and the Cardiac Arrest Study, Hamburg (CASH), demonstrated better survival with ICD therapy than with antiarrhythmic therapy with amiodarone or sotalol. The survival difference was statistically significant in AVID, of borderline significance in CIDS, and insignificant in CASH. A meta-analysis of the 3 trials found a 28% reduction in relative risk of death. [57]

Current guidelines also recommend ICD placement in patients with nonischemic dilated cardiomyopathy and considerable left ventricular dysfunction, or arrhythmogenic right ventricular cardiomyopathy, who have sustained VT or VF. These patients should be receiving optimal long-term medical therapy and may reasonably be expected to survive with good functional status for more than 1 year. [1]

ICDs are not used for the following [30] :

  • Patients with VT or VF occurring during an acute ST-segment elevation MI (STEMI)
  • Patients with reversible, drug-induced VT
  • Patients with poor expected survival as a consequence of comorbid conditions

Because ICDs treat, rather than prevent, ventricular arrhythmias, as many as 50% of ICD recipients require therapy with antiarrhythmic drugs to reduce the potential for ICD shocks. The 2006 ACC/AHA/ESC guidelines support the use of catheter ablation in patients with an ICD who are receiving multiple shocks because of sustained VT that is not manageable by changing drug therapy or who do not wish to undergo long-term drug therapy. [25]

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Diet and Activity

Patients with ischemic VT may benefit from low-cholesterol diets, low-salt diets, or both. Patients with idiopathic VT may notice a reduction in symptoms when stimulants (eg, caffeine) are avoided. [58] Fish oil supplementation does not reduce the risk of VT or VF in ICD patients with recent sustained ventricular arrhythmia. [59]

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, ablation therapy, or some combination thereof.

The 2006 ACC/AHA/ESC guidelines recommend that smoking be strongly discouraged in all patients who have, or who are thought to have, ventricular arrhythmias, aborted sudden cardiac death (SCD), or both. Cigarette smoking is an independent risk factor for SCD, typically from arrhythmia and regardless of underlying coronary heart disease, and smoking cessation significantly reduces the risk of SCD. [25]

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Consultations

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

In rare cases, a patient with a stable, recurrent episode of VT that is controlled in the ED can be discharged rather than admitted, provided that appropriate follow-up care is available. However, this decision must be made in consultation with a cardiologist.

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Long-Term Monitoring

Outpatient medication choices depend on the degree of ventricular dysfunction, the presence or absence of an ICD, and the presence or absence of comorbid disease, such as asthma. Continued therapy for underlying heart failure or coronary artery disease (CAD) remains important.

Patients receiving long-term antiarrhythmic therapy should be observed regularly for proarrhythmia and adverse effects. Patients should be questioned carefully about recurrent palpitations and syncope. 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 testing guidelines. [25]

Sotalol is loaded on an inpatient basis, with telemetry and electrocardiographic (ECG) monitoring during 5-6 drug half-lives for bradycardia, ventricular proarrhythmia, and excessive QT prolongation. Many centers then follow sotalol patients on a quarterly basis to reassess renal function, observe QT intervals, and watch for new drug interactions.

When VT is observed in a patient receiving an antiarrhythmic drug, it is essential to distinguish between VT recurrence and drug-induced ventricular proarrhythmia. The most common malignant form of proarrhythmia is torsades de pointes associated with QT-interval prolongation, usually due to excessive potassium-channel blockade.

The possibility of drug-specific noncardiac adverse effects warrants special vigilance. For example, flecainide can cause visual disturbances. Procainamide can cause joint pains and (with long-term use) a lupus syndrome.

Patients with ICDs require regular outpatient device follow-up to allow monitoring of battery and transvenous lead status. Although battery lifetime is somewhat predictable, lead fracture and failure may occur at any time. Lead problems can generally be diagnosed in the clinic and occasionally necessitate lead revision or replacement.

In addition, the efficacy of the ICD should be rechecked after the initiation of medications that may increase the ventricular defibrillation threshold. This is typically accomplished by means of an outpatient noninvasive programmed stimulation study (NIPS) carried out through the implanted device.

The ACC/AHA/ESC guidelines advise that patients who have experienced polymorphic VT in association with a prolonged QT interval as a result of antiarrhythmic agents or other drugs should be cautioned to avoid exposure to all agents associated with QT prolongation. A list of such agents can be found at the ArizonaCERT website. [25]

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