Ventricular Tachycardia Treatment & Management

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:

• 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 (LV) function is normal or impaired (eg, reduced LV ejection fraction [LVEF], heart failure).

In stable patients with monomorphic VT and normal LV function, restoration of sinus rhythm is typically achieved with intravenous (IV) procainamide, amiodarone, or sotalol. Lidocaine may also be used, but this agent may have common and limiting side effects and, consequently, increase the overall mortality risk. A 12-lead electrocardiogram (ECG) is obtained before conversion.

If LV 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. ^{[52, 53, 54, 55]} 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. Administration of 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. ^[40]

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 anti-digitalis antibody may be indicated. ^[40]

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 ^{[9, 14]} :

• Antiarrhythmic medications: Effective in reducing the arrhythmia burden but have no demonstrated mortality benefit ^[9] ; however, results from the Amiodarone, Lidocaine, or Placebo (ALPS) study indicate poor but not invariably fatal outcomes from the use of amiodarone or lidocaine for nonshockable (asystole/pulseless electric activity)-turned-shockable (ventricular fibrillation/VT) out-of-hospital cardiac arrest during resuscitation ^[56]
• Implantable cardioverter-defibrillator (ICD): Aids in the acute termination of ventricular arrhythmia and provides information on the long-term management of patients with VT ^[9]
• Catheter ablation: Effective, but recurrent VT is not uncommon ^{[9, 57, 58]}

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. ^[59]

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 its high mortality and the advent of ICDs and ablative therapies.

Select 2017 AHA/ACC/HRS recommendations

Select recommendations from the 2017 American Heart Association (AHA)/American College of Cardiology (ACC)/Heart Rhythm Society (HRS) guideline for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death include the following ^[44] :

• Patients with heart failure and reduced LVEF (≤40%): Administer a beta blocker, mineralocorticoid receptor antagonist, and either an angiotensin-converting enzyme inhibitor (ACEI) or an angiotensin-receptor blocker (ARB), or an angiotensin receptor-neprilysin inhibitor (ARNI) to reduce the risk of sudden cardiac death and all-cause mortality.
• Patients with ischemic heart disease and sustained monomorphic VT: More than coronary revascularization alone is needed to prevent recurrent VT.
• Patients with nonischemic cardiomyopathy, symptomatic heart failure (New York Heart Association [NYHA] class II-III symptoms), and an LVEF of 35% or below while on guideline-directed therapy: Place an ICD if the expected survival is longer than 1 year.
• Patients with previous MI and recurrent symptomatic sustained VT, or present with VT/VF storm, and are refractory to/intolerant of amiodarone: Perform catheter ablation.
• Patients requiring arrhythmia suppression for symptoms or declining ventricular function probably owing to frequent premature ventricular complexes for whom antiarrhythmics are not effective, tolerated, or preferred: Catheter ablation provides benefit.

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 electrocardiographic rhythm strip monitoring are all-important, but they should not delay rapid transport to the ED for definitive care.

The acute emphasis in patients with ventricular tachycardia (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. ^{[60, 61, 62]}  Please refer to the most current ACLS guidelines, which are subject to periodic revision.

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. ^[63] Although intravenous (IV) lidocaine is effective at suppressing peri-infarction VT, it may increase the overall mortality risk. In situations involving torsade 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. This tracing is from a patient with a structurally normal heart who has a normal resting electrocardiogram. This rhythm is orthodromic reciprocating tachycardia with rate-related left bundle-branch block. Note the relatively narrow RS intervals in the precordial leads.

View Media Gallery

This electrocardiogram is from a 48-year-old man with wide-complex tachycardia during a treadmill stress test. Any wide-complex tachycardia tracing should raise the possibility of ventricular tachycardia, but closer scrutiny confirms left bundle-branch block conduction of a supraventricular rhythm. By Brugada criteria, RS complexes are apparent in the precordium (V2-V4), and the interval from R-wave onset to the deepest part of the S wave is shorter than 100 ms in each of these leads. Ventriculoatrial dissociation is not seen. Vereckei criteria are based solely upon lead aVR, which shows no R wave, an initial q wave width shorter than 40 ms, and no initial notching in the q wave. The last Vereckei criterion examines the slope of the initial 40 ms of the QRS versus the terminal 40 ms of the QRS complex in lead aVR. In this case, the initial downward deflection in lead aVR is steeper than the terminal upward deflection, yielding Vi/Vt ratio above 1. All of these criteria are consistent with an aberrantly conducted supraventricular tachycardia. Gradual rate changes during this patient's treadmill study (not shown here) were consistent with a sinus tachycardia mechanism.

View Media Gallery

If the clinical situation permits, a 12-lead electrocardiogram (ECG) should be obtained before conversion of the rhythm. The ECG criteria of Brugada et al ^[15] 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. ^[19]

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. ^[64]  

After initial treatment and stabilization, patients with ventricular tachycardia (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 torsade 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 is necessarily completed on an outpatient basis. ^[55]

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.

Adult patients with ventricular arrhythmias whose age, sex, and symptoms indicate a moderate or greater likelihood of coronary heart disease, should undergo exercise testing to provoke ischemic changes or ventricular arrhythmias. ^[40] 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. ^[40]

Patients with monomorphic ventricular tachycardia (VT) who have structurally normal hearts are at a low risk of sudden death. Consequently, implantable cardioverter-defibrillators (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. ^[65]

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.

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. ^[40]

In the Electrophysiologic Study versus Electrocardiographic Monitoring (ESVEM) trial, which compared long-term treatment with seven 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. ^[65] 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

Statin therapy is advantageous in patients with coronary heart disease, to reduce the risk of vascular accidents, ventricular arrhythmias (possibly), and sudden cardiac death. ^[40]

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. ^[54]

Radiofrequency ablation (RFA) via endocardial or epicardial catheter placement can be used to treat ventricular tachycardia (VT) in patients with left ventricular dysfunction from previous myocardial infarction (MI), ^[66] cardiomyopathy, bundle-branch reentry, and various forms of idiopathic VT (see the image below). ^[40]  RFA is often used in conjunction with implantable cardioverter-defibrillator (ICD) therapy in the presence of recurrent VT episodes to reduce the frequency of required ICD therapies. ^[40] For patients with structural heart disease, it is currently uncertain whether VT ablation obviates other therapies, such as placement of an ICD). ^{[5, 6, 7, 8]}

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

View Media Gallery

Current techniques include three-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. ^{[67, 68]}

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. ^[40] 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 the arrhythmia burden and thereby minimize the number of ICD shocks.

Ablation is also used in patients with bundle-branch reentrant VT. ^[40] 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.

Kumar et al assessed the long-term prognosis after ablation for sustained VT in 695 consecutive patients with no structural heart disease (no SHD, n = 98), ischemic cardiomyopathy (ICM, n = 358), or nonischemic cardiomyopathy (NICM, n = 239). At a median follow-up of 6 years, ventricular arrhythmia (VA)-free survival was highest in patients with no SHD (77%), followed by patients with ICM (54%) and patients with NICM (38%); overall survival was highest in patients with no SHD (100%), followed by patients with NICM (74%) and patients with ICM (48%). ^[69]

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. ^[70]  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 1 year, with 90% cardiac transplantation-free survival  at 1 year in those without VT recurrence, compared with 71% in patients with recurrence. ^[70]

In a two-center study that examined the use of a percutaneous left ventricular assist device (pLVAD) in patients undergoing ablation for scar-related VT, use of a pLVAD allowed maintenance in VT for a significantly longer period by virtue of its ability to maintain end-organ perfusion. ^[71]  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. ^[72]

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). ^{[73, 74]}

Posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a previous septal myocardial infarction. The earliest activation is recorded in red, and late activation 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.

View Media Gallery

In a study that evaluated the long-term safety and effectiveness of irrigated radiofrequency catheter ablation in 249 patients with sustained monomorphic VT associated with coronary disease, 75.9% achieved noninducibility of targeted VT. ^[75] The results showed that RFA reduced ICD shocks and VT episodes and improved quality of life at 6 months; improved long-term outcomes included a steady 3-year nonrecurrence rate with reduced amiodarone use and hospitalizations. ^[75]

In a prospective study to assess the incidence and predictors of major complications from contemporary catheter ablation procedures, major complication rates ranged from 0.8% (SVT) to 6% (VT associated with structural heart disease), depending on the ablation procedure performed. ^[76]  Renal insufficiency was the only independent predictor of a major complication.

The advent of 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 implanted, the ICD can detect ventricular tachyarrhythmias and terminate them with defibrillation shocks or anti-tachycardia pacing algorithms (see the image below).

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

View Media Gallery

ICD therapy is used to augment medical management for the following individuals ^[4] :

• Most patients with hemodynamically unstable VT
• Most patients with prior myocardial infarction (MI) and hemodynamically stable sustained VT
• Most cardiomyopathy patients with unexplained syncope (an arrhythmia is presumed)
• 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. ^[77] The survival difference was statistically significant in AVID, of borderline significance in CIDS, and insignificant in CASH. A meta-analysis of the three trials found a 28% reduction in relative risk of death. ^[77]

Patients with nonischemic dilated cardiomyopathy and considerable left ventricular dysfunction, or arrhythmogenic right ventricular cardiomyopathy, who have sustained VT or VF should have ICD placement. These patients should also be receiving optimal long-term medical therapy and may reasonably be expected to survive with good functional status for longer than 1 year. ^[4]

ICDs are not used for the following individuals ^[46] :

• 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. Catheter ablation may be used 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. ^[40]

Prospective follow-up data from 2,352 patients in the Israeli ICD Registry suggest that the presence of anemia (hemoglobin [Hb] ≤12 g/dL) in patients with ICDs independently increases the risk for ventricular arrhythmias during long-term follow-up. ^[78]  At 2.5 years of follow-up, the rate of appropriate shocks in patients with low Hb levels (11%) was nearly double that of those with high Hb levels (6%) (log-rank P <0.005). Moreover, each 1 g/dL reduction in Hb was independently associated with a significant 8% increased risk for a first appropriate shock (P <0.03), and anemia increased the risk for all-cause mortality as well as heart failure hospitalizations or death, but not with inappropriate ICD shocks. ^[78]

Patients with ischemic ventricular tachycardia (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. ^[79] Fish oil supplementation does not reduce the risk of VT or VF in patients with implantable cardioverter-defibrillator (ICD) and a recent sustained ventricular arrhythmia. ^[80]

VT may be precipitated by increased sympathetic tone during strenuous physical exertion. A 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.

Smoking should 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; smoking cessation significantly reduces the risk of SCD. ^[40]

Patients with ventricular tachycardia (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 emergency department 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.

Outpatient medication choices for patients with ventricular tachycardia (VT) depend on the degree of ventricular dysfunction, the presence or absence of an an implantable cardioverter-defibrillator (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. ^[40]

Sotalol and dofetilide are 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-receiving patients on a quarterly basis to reassess renal function, observe QT intervals, and watch for new drug interactions. Patients with frequent VT episodes (“storm”) receiving amiodarone also commonly receive at least an initial load during an inpatient status via an intravenous route.

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 torsade 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.

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 Arizona Center for Education and Research on Therapeutics (AZCERT) website.