Ventricular Tachycardia Treatment & Management
- Author: Steven J Compton, MD, FACC, FACP; Chief Editor: Jeffrey N Rottman, MD more...
Prehospital Care
Rapid transport to an ED is essential.
Emergency medical technicians (EMTs) and paramedics may be called upon to provide cardioversion/defibrillation in the field if they have sufficient training and if appropriate protocols exist.
Emergency medical service (EMS) personnel must pay adequate attention to the primary survey and address the ABCs 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.
Approach Considerations
The mainstays of treatment for clinically stable ventricular tachycardia (VT) are the various antidysrhythmic drugs.
Patients with VT may suffer congestive heart failure and its attendant morbidity as a result of hemodynamic compromise.
VT may deteriorate to ventricular fibrillation (VF).
Consider all patients with VT to have active myocardial ischemia, which should be treated aggressively.
In the past, long-term antidysrhythmic medical therapy was used for the suppression of VT. However, several subsets of patients with VT do poorly under such an approach, with frequent recurrence of VT. As a result, cardiologists are increasingly making use of interventional therapy, with devices and procedures designed to abort VT or to remove the dysrhythmogenic foci in the heart.
According to the ACC/AHA/ESC 2006 guidelines, coronary revascularization is indicated to reduce the risk of SCD in patients with VF when direct evidence of acute myocardial ischemia is known to immediately precede the onset of VF.[16]
Sustained ventricular tachycardia (VT) may precede a significant hemodynamic collapse. When this rhythm is present, it should be addressed rapidly.
Go to Pediatric Ventricular Tachycardia for complete information on this topic.
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 ACLS protocols.
Stable VT denotes monomorphic VT with adequate vital end-organ perfusion. These patients do not experience signs/symptoms of hemodynamic compromise.
If the hemodynamic status is stable and no evidence of 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, the use of amiodarone, then lidocaine, has been favored over procainamide because of the latter drug's potential for exacerbating congestive heart failure.
However, mounting evidence indicates that amiodarone should not be the first-line antidysrhythmic in the treatment of stable VT, because its effects on myocardial conduction and refractoriness are gradual in onset.[24, 25, 26, 27]
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.
The ACC/AHA/ESC 2006 guidelines advise that patients who experience polymorphic VT in association with prolonged QT interval due to 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.[16]
Efforts should be made to correct hypokalemia and withdraw any chronic medications associated with QT-interval prolongation.
When associated with ongoing myocardial ischemia, lidocaine is suggested as the primary antidysrhythmic medication, because the mechanism is thought to be abnormal automaticity and not reentry.[21, 28] In situations involving torsade de pointes, magnesium sulfate may be effective if a long QT interval is present at baseline. The ACC/AHA/ESC 2006 guidelines state that magnesium is not likely to be effective in patients with a normal QT interval.[16] Consider synchronized cardioversion early if medical therapy fails to stabilize the rhythm. Initial shock energy should be 100 J (monophasic), followed by higher shock energies if the response is inadequate.
In accordance with the ACC/AHA/ESC 2006 guidelines, cardioversion with sedation as necessary is recommended for patients with sustained polymorphic VT with hemodynamic compromise. Use of this intervention is reasonable at any point during treatment.[16]
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), seen in the ECGs below. 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.
Supraventricular tachycardia (SVT) with aberrancy This is a patient with a structurally normal heart who has a normal resting ECG. This rhythm is an orthodromic reciprocating tachycardia with a rate-related left bundle branch block. Note the relatively narrow RS intervals in the precordial leads. 
This ECG is from a 48-year-old male with wide complex tachycardia during treadmill stress test. Any wide complex tachycardia tracing should raise the possibility of VT, but closer scrutiny confirms left bundle branch block conduction of a supraventricular rhythm. Starting with the Brugada criteria, RS complexes are apparent in the precordium (V2-V4), and the interval from the R wave onset to the deepest part of the S wave is < 100 msec in each of these leads. Ventriculoatrial dissociation is not seen. See Brugada et al (1991) for details of additional morphologic criteria. The Vereckei criteria (2008) are based solely upon aVR, which shows no R wave, an initial q wave width < 40 ms, and no initial notching in the q wave. The last criterion by Vereckei et al examines the slope of the initial 40 ms of the QRS versus the terminal 40 ms of the QRS complex in aVR. In this case, the initial downward deflection in aVR is steeper than the terminal upward deflection, giving a vi/vt ratio >1. All of these criteria are consistent with aberrantly conducted SVT. The 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 prior to conversion of the rhythm. The ECG criteria of Brugada et al[22] may be useful in differentiating the arrhythmia mechanism, as outlined previously.
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.[4]
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. During the initial assessment, once real-time cardiac monitoring or 12-lead ECG has established VT as the diagnosis, one should determine if the VT is stable or unstable as the ABCs are reassessed in the primary survey.
Unstable VT is characterized by signs/symptoms of insufficient oxygen delivery to vital organs. These signs/symptoms can be chest pain, dyspnea, hypotension, and an altered level of consciousness, which indicate that heart rate and contractility are not enabling adequate cardiac output.
In this situation, the dysrhythmia should be immediately treated with synchronized cardioversion, usually at a starting energy dose of 100 J (monophasic). Comparable biphasic recommendations are not available at this time.
In contrast, 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.
Pulseless VT
Pulseless VT, in contrast to other unstable VT rhythms, is treated with immediate defibrillation. High-energy, unsynchronized energy should be used. The initial shock dose on a biphasic defibrillator is 150-200 J, followed by an equal or higher shock dosage for subsequent shocks. If a monophasic defibrillator is used, the initial and subsequent shock dosage should be 360 J. Shock administration should be followed by immediate chest compressions, airway management with supplemental oxygen, and vascular access with administration of vasopressor agents. In cases of shock-resistant pulseless VT, one can consider use of antidysrhythmic medications.
Vasopressors can include epinephrine at 1 mg IV given every 3-5 minutes, or in lieu of epinephrine, vasopressin 40 U IV as a 1-time dose.
ACLS drug-therapy guidelines recommend the use of intravenous amiodarone or lidocaine as the first-line adjunctive, antidysrhythmic treatment of shock-resistant pulseless VT.
Ventricular Tachycardia Postconversion
Following conversion of ventricular tachycardia (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.[29] 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.
The ECG below is from a patient who underwent catheter ablation.
Curative ablation of ventricular tachycardia (VT). This patient has VT in the setting of an ischemic cardiomyopathy. His VT was induced in the electrophysiology laboratory, and an ablation catheter was placed at a critical zone of slow conduction within the VT circuit. Radiofrequency (RF) energy is applied to the tissue through the catheter tip, and VT terminates when the critical conducting tissue is destroyed. 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.
As per the ACC/AHA/ESC 2006 guidelines, when used in combination with beta blockers, amiodarone can be useful for patients with LV dysfunction due to prior MI and symptoms due to VT that do not respond to beta-adrenergic-blocking agents.[16]
In the setting of congestive heart failure, the best proven, but nonspecific, antiarrhythmic drug strategies include the use of beta receptor–blocking drugs carvedilol, metoprolol, and bisoprolol; angiotensin-converting enzyme (ACE) inhibitors; and aldosterone antagonists. According to the ACC/AHA/ESC 2006 guidelines, statin therapy is advantageous in patients with CHD to reduce the risk of vascular accidents, possibly ventricular arrhythmias, and SCD.[16]
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 (see the ECG below).
The ACC/AHA/ESC 2006 guidelines recommend ICD therapy for primary prevention to reduce total mortality by a reduction in SCD in patients with LV dysfunction due to previous MI who are at least 40 days post-MI, have an LVEF less than or equal to 30-40%, are NYHA functional class II or III, are receiving chronic optimal medical therapy, and who can reasonably be expected to survive with good functional status for more than 1 year.[16] ICD is also effective in reducing mortality by a reduction in SCD in patients with LV dysfunction due to prior MI who present with hemodynamically unstable sustained VT.[16]
The ACC/AHA/ESC guidelines also state that it is reasonable to implant an ICD in patients with LV dysfunction due to prior MI who are at least 40 days post-MI, have an LVEF less than or equal to 30-35%, are NYHA functional class I and receiving ongoing optimal medical care, and who can reasonably be expected to survive with good functional status for more than 1 year.[16]
Termination of ventricular tachycardia (VT) with overdrive pacing. This patient has a reentrant VT, which is terminated automatically by pacing from an implantable cardioverter-defibrillator (ICD). 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, 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 than in those taking antiarrhythmic drugs (amiodarone and sotalol were used). The survival difference was significant in AVID, of borderline statistical significance in CIDS, 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.[30]
As stated by the 2006 ACC/AHA/ESC guidelines, implantation of an ICD along with use of beta blockers is recommended for patients with long QT syndrome (LQTS) who have had a previous cardiac arrest and who can be reasonably expected to survive with a good functional status for more than 1 year.[16]
Lifestyle modification is recommended for patients with LQTS, along with the use of beta blockers.
Catheter Ablation
Endocardial catheter ablation is used early in idiopathic monomorphic VT (ie, VT in a 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.
The ACC/AHA/ESC 2006 guidelines recommend ablation in patients who are otherwise at low risk for SCD and have sustain predominantly monomorphic VT that is drug resistant, in those who are drug intolerant, or in those who do not wish long-term drug therapy.[16]
The ACC/AHA/ESC guidelines also recommend catheter ablation in patients with structurally normal hearts with symptomatic, drug-resistant VT due to RV or LV or in those who are drug intolerant or who refuse long-term drug therapy.
In some patients, percutaneous epicardial ablation can be used successfully when endocardial lesions fail. Current techniques include 3-dimensional scar, isopotential, and activation mapping, followed by high-energy radiofrequency ablation with irrigated-tip catheters capable of creating deeper lesions in the thicker left ventricular wall.
The ACC/AHA/ESC guidelines recommend ablation in patients with bundle-branch reentrant VT.[16] 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.
A 2-center study examined the use of a percutaneous left ventricular assist device (pLVAD) in patients undergoing scar-related VT ablation. Use of a pLVAD allowed for maintenance in VT for significantly longer due to an ability to maintain end-organ perfusion. Whether this will translate into clinical benefits is unclear, but this study at least demonstrates the benefit of pLVADs in patients with scar-related, unstable VT.[31]
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. Difficulty of outflow tract ablation may be predicted by electrocardiographic morphology.[32]
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.[33]
This is a posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a prior septal myocardial infarction. Earliest activation is recorded in red; late activation shows as blue to magenta. Fragmented low amplitude diastolic local electrograms were recorded adjacent to the 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. Major complication rates ranged between 0.8% (supraventricular tachycardia) and 6% (VT associated with structural heart disease ), depending on the ablation procedure performed. They reported renal insufficiency was the only independent predictor of a major complication.[34]
Infarct Zone Incision
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 ICDs and ablative therapies.
Diet
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.
Activity
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.
The ACC/AHA/ESC 2006 guidelines recommend that smoking be strongly discouraged in all patients who have, or who are thought to have, ventricular arrhythmias and/or aborted SCD.
Inpatient Care in Ventricular Tachycardia
Following initial treatment and stabilization, patients with ventricular tachycardia (VT) generally should be referred to a cardiologist for admission to a monitored bed; further studies, such as electrophysiologic study (EPS) with possible radiofrequency ablation; and possible automatic internal cardioverter/defibrillator (AICD) placement.
Outpatient Care in Ventricular Tachycardia
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.
Treatment Concerns and Monitoring
Inpatients
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.[35]
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 ACC/AHA/ESC 2006 guidelines recommend exercise testing in adult patients with ventricular arrhythmias who have a moderate or greater chance of having CHD by age, gender, and symptoms to provoke ischemic changes or ventricular arrhythmias.[16] Regardless of age, exercise testing is useful in patients with established or suspected exercise-induced VAs, including catecholaminergic VT, to provoke the arrhythmia, to confirm a diagnosis, and to ascertain the patient’s response to tachycardia.[16]
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.
Outpatients
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.[16]
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 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 ICD should be rechecked following the 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.
Because most patients with ventricular tachycardia have an underlying cardiomyopathy, continued therapy of congestive heart failure and coronary artery disease remains important.
The ACC/AHA/ESC 2006 guidelines recommend ICD therapy for secondary prevention of SCD in patients with heart failure who survived VF or hemodynamically unstable VT, or VT with syncope and who have an LVEF less than or equal to 40%, who are receiving ongoing optimal medical treatment, and who are reasonably expected to survive with a good functional status for more than 1 year.[16]
The ACC/AHA/ESC guidelines also recommend ICD therapy for primary prevention to reduce total mortality by a reduction in SCD in patients with LV dysfunction due to previous MI who are at least 40 days post-MI, have an LVEF less than or equal to 30-40%, are NYHA functional class II or III, are receiving ongoing optimal medical care, and who can reasonably be expected to survive with good functional status for more than 1 year.[16]
Consultations
Cardiac electrophysiology is a subspecialty devoted to the diagnosis and management of cardiac arrhythmias. Patients with ventricular tachycardia (VT) should be referred to general cardiologists or electrophysiologists for specialized care.
Only rarely will a patient with stable, recurrent episodes of VT have his or her dysrhythmia treated in the ED and be discharged with appropriate follow-up care. This decision must be made in consultation with a cardiologist.
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