Ventricular Tachycardia

Ventricular tachycardia (VT) refers to any rhythm faster than 100 (or 120) beats/min arising distal to the bundle of His. It is the most common form of wide complex tachycardia, with a high associated mortality rate.[9] The rhythm may arise from the working ventricular myocardium, the distal conduction system, or both. (See Etiology.) VT can be classified as sustained or nonsustained, with a generally accepted cutoff of 30 seconds.

VT is further classified according to the electrocardiographic (ECG) appearance. If the QRS complex remains identical from beat to beat, as occurs when VT originates from a single focus or circuit, it is classified as monomorphic (see the first two images below). If the QRS morphology changes from beat to beat, the VT is classified as polymorphic (see the third image below). Further classification can be made on the basis of the substrate and the location of the earliest activation.

This electrocardiogram (ECG) shows rapid monomorphic ventricular tachycardia (VT), 280 beats/min, associated with hemodynamic collapse. The tracing was obtained from a patient with severe ischemic cardiomyopathy during an electrophysiologic study. A single external shock subsequently converted VT to sinus rhythm. The patient had an atrial rate of 72 beats/min (measured with intracardiac electrodes; not shown). Although ventriculoatrial dissociation (faster V rate than A rate) is diagnostic of VT, surface ECG findings (dissociated P waves, fusion or capture beats) are present in only about 20% of cases. In this tracing, the ventricular rate is simply too fast for P waves to be observed. VT at 240-300 beats/min is often termed ventricular flutter.

This electrocardiogram shows slow monomorphic ventricular tachycardia (VT), 121 beats/min, from a patient with an old inferior wall myocardial infarction and well-preserved left ventricular (LV) function (ejection fraction, 55%). The patient presented with symptoms of palpitation and neck fullness. Note the ventriculoatrial dissociation, which is most obvious in leads V2 and V3. Slower VT rates and preserved LV function are associated with better long-term prognosis.

This image demonstrates polymorphic ventricular tachycardia.

In the United States, the most common setting for VT is ischemic heart disease, in which myocardial scar tissue is the substrate for electrical reentry. VT can also be seen in other conditions that create a myocardial scar, such as the following (see Etiology):

• Dilated cardiomyopathy
• Hypertrophic cardiomyopathy
• Arrhythmogenic right ventricular dysplasia (ARVD) or cardiomyopathy
• Chagas disease ^[10]
• Surgical incisions in the ventricle

VT may also occur in the absence of structural heart disease. VT in this setting may result from enhanced automaticity, which most commonly originates in the right ventricular outflow tract or from the fascicles of the cardiac conduction system. Bundle-branch reentrant VT occurs in patients with conduction system disease distal to the bundle of His. Finally, functional reentrant VTs can occur in structurally normal hearts, in patients with inherited channelopathies.[11]  The VT morphology can provide a guide to the anatomic likely site of origin in the heart.[12, 13]

VT can also be triggered by the following (see Etiology):

• Electrolyte deficiencies (eg, hypokalemia, hypocalcemia,  hypomagnesemia)
• Systemic diseases that affect the myocardium (eg, sarcoidosis, amyloidosis, systemic lupus erythematosus, hemochromatosis, rheumatoid arthritis)
• Sympathomimetic agents, including intravenous (IV) inotropes and illicit drugs such as methamphetamine or cocaine
• Digitalis toxicity, which can lead to biventricular tachycardia
• Drugs that prolong the QT interval (class IA and class III antiarrhythmics, azithromycin, levofloxacin, and many others); these may cause torsade de pointes
• Drugs that slow conduction velocity, particularly when an underlying myocardial scar is present (eg, halothane and class IA and IC antiarrhythmics)

Clinically, VT may be reflected in symptoms such as syncope, palpitations, and dyspnea (see Presentation). It is often, but not always, associated with hemodynamic compromise, particularly if the left ventricle is impaired or the heart rate is especially fast. With some exceptions, VT is associated with increased risk of sudden death.[1, 14] (See Prognosis.)

The ECG diagnosis of VT is generally straightforward, but it does require that this condition be distinguished from aberrantly conducted supraventricular tachycardia (SVT), which has a similar ECG pattern. ECG criteria for confirming the presence of a VT mechanism for a wide-complex tachycardia include the following:

• Presence of atrioventricular (AV)—technically, ventriculoatrial—dissociation (in which the ventricles fire at a faster rate than the atria)
• Fusion beats
• Capture beats

Because AV dissociation, fusion, and capture beats occur in only a minority of VT tracings, additional 12-lead ECG criteria (the Brugada criteria[15] and the Vereckei criteria[16] ) have been derived to facilitate discrimination between VT and aberrantly conducted SVT. (See Workup).

Accelerated idioventricular rhythm, sometimes termed slow VT, is a variant of VT that produces a rate of 60-120 beats/min. It typically occurs in patients with underlying heart disease (ischemic or structural), is transient, and only rarely is associated with hemodynamic compromise or collapse. Treatment of the dysrhythmia itself usually is not required unless significant hemodynamic impairment develops.

Patients with frank hemodynamic compromise from acute VT require emergency management with electrical cardioversion. Although cardioversion treats VT, it does not prevent recurrence of VT, and patients may experience repeated episodes of recurrent VT after cardioversion; this phenomenon is termed VT storm. These patients additionally require acute antiarrhythmic therapy, ablation therapy, or both.

The mainstays of long-term treatment for clinically stable patients with VT are the various antiarrhythmic drugs. However, cardiologists are increasingly making use of interventional therapy with devices and ablation procedures designed to abort VT or to destroy arrhythmogenic tissue in the heart. (See Treatment.)

For information on VT in children, see Pediatric Ventricular Tachycardia. For patient education information, see the Heart Health Center, as well as Arrhythmias (Heart Rhythm Disorders), Supraventricular Tachycardia (SVT, PSVT), and Palpitations.

At the cellular level, ventricular tachycardia (VT) is caused by electrical reentry or abnormal automaticity. Myocardial scarring from any process increases the likelihood of electrical reentrant circuits. These circuits generally include a zone where normal electrical propagation is slowed by the scar. Ventricular scar formation from a prior myocardial infarction (MI) is the most common cause of sustained monomorphic VT.

VT in a structurally normal heart typically results from mechanisms such as triggered activity and enhanced automaticity. Torsade de pointes, seen in the long QT syndromes, is likely a combination of triggered activity and ventricular reentry.[17]

During VT, cardiac output is reduced as a consequence of decreased ventricular filling from the rapid heart rate and the lack of properly timed or coordinated atrial contraction. Ischemia and mitral insufficiency[18] may also contribute to decreased ventricular stroke output and hemodynamic intolerance.

Hemodynamic collapse is more likely when underlying left ventricular dysfunction is present or when heart rates are very rapid. Diminished cardiac output may result in diminished myocardial perfusion, worsening inotropic response, and degeneration to ventricular fibrillation (VF), resulting in sudden death.

In patients with monomorphic 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 degeneration of monomorphic or polymorphic VT to VF.[10] Even without such degeneration, VT can also produce congestive heart failure and hemodynamic compromise, with subsequent morbidity and mortality.

If VT is hemodynamically tolerated, the incessant tachyarrhythmia may cause a dilated cardiomyopathy. This may develop over a period of weeks to years and may resolve with successful suppression of the VT.[19] A similar course is occasionally seen in patients with frequent premature ventricular contractions or ventricular bigeminy, despite the absence of sustained high rates.[20]

Causes of ventricular tachycardia (VT) include the following[11] :

• Ischemic heart disease (most common)
• Structural heart disease with disruption of normal conduction patterns (eg, nonischemic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy [ARVD] or cardiomyopathy, hypertrophic cardiomyopathy)
• Congenital structural cardiac disorders (eg, tetralogy of Fallot) and associated surgical scar
• Acquired channelopathies, most commonly from drugs that prolong the QT interval (eg, class IA and class III antiarrhythmics, phenothiazines, methadone, many others); drugs that slow myocardial conduction (eg, flecainide, propafenone, halothane) may also promote reentrant VT
• Inherited channelopathies (eg, long QT syndrome, short QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia)
• Electrolyte imbalances (eg, hypokalemia, hypocalcemia,  hypomagnesemia)
• Sympathomimetic agents, including intravenous (IV) inotropes and illicit drugs such as methamphetamine or cocaine
• Digitalis toxicity, which can lead to biventricular tachycardia
• Systemic diseases causing infiltrative cardiomyopathy or scar (eg, sarcoidosis, amyloidosis, systemic lupus erythematosus, hemochromatosis, rheumatoid arthritis)

Hypokalemia is an important arrhythmia trigger, followed by hypomagnesemia. Hyperkalemia may also predispose to VT and ventricular fibrillation (VF), particularly in patients with structural heart disease. Other triggers include sleep apnea and atrial fibrillation (AF), which can increase VT risk in patients with preexisting structural heart disease.

QT prolongation, which may be acquired or inherited, can lead to VT. Acquired QT prolongation is observed with certain potassium channel–blocking medications. Most of the causative drugs block the delayed rectifier cardiac potassium current, IKr. These agents include class IA and class III antiarrhythmics, azithromycin, and many others. 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, a reentrant rhythm with a constantly varying circuit.[17] Other inherited ion channel abnormalities may cause idiopathic VF and familial polymorphic VT in the absence of QT prolongation.

Although the following syndromes have been described in most parts of the world, population groups in certain regions carry locally increased risk of genetically mediated heart disease. Examples include the Veneto region of Italy and the Greek island of Naxos (right ventricular dysplasia),[21] as well as northeastern Thailand (idiopathic VF/Brugada syndrome).[22] The risk for VT within populations varies primarily with the risk factors for atherosclerosis, however, rather than with ethnic differences per se.

Among patients younger than 35 years, the most common cardiac causes of sudden death, and presumably of VT, include the following[23] :

• Hypertrophic cardiomyopathy
• Right ventricular cardiomyopathy (ARVD)
• Myocarditis
• Long QT syndrome
• Congenital coronary artery abnormalities

Inherited long QT syndrome

Long QT syndrome is characterized by QT interval prolongation, T-wave abnormalities, and polymorphic VT. Persons with this syndrome are predisposed to episodes of polymorphic VT. These episodes can be self-limited, resulting in syncope, or they may transition into VF and thus can cause sudden cardiac death.

Long QT syndromes have been identified by eponyms (ie, Romano-Ward syndrome, Jervell and Lange-Nielsen syndrome, Andersen-Tawil syndrome,[24] and Timothy syndrome[25] ). The form sometimes known as Romano-Ward syndrome is the most common type. However, current practice is moving away from using eponyms and toward denoting these syndromes as numbered types (eg, LQT1 through LGT12) on the basis of identified underlying mutations.

Mutations in the KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2 genes are known to be causative. Together, those five genes are responsible for virtually 100% of cases of inherited long QT syndrome.

Catecholaminergic polymorphic ventricular tachycardia

Catecholaminergic polymorphic VT (CPVT) is characterized by polymorphic VT that can be triggered by stress, exercise, or even strong emotional states. It can be induced by catecholamine administration. Patients may present with syncope or with sudden cardiac death if the dysrhythmia degrades into VF. Physical examination or electrocardiography (ECG) during rest will likely be normal.

CPVT may be caused by mutations in the CASQ2 or RYR2 genes.[26] An additional locus has been mapped to chromosome 7p22-p14. This disorder shares clinical characteristics with the bidirectional VT sometimes seen in digitalis toxicity.

Dilated cardiomyopathy

Dilated cardiomyopathy is a highly heterogeneous disorder that can predispose to ventricular tachyarrhythmias such as VT. Its genetic causes are myriad and involve mutations in genes coding for proteins that make up cardiac sarcomeres, including actin, myosin, and troponin. It is noteworthy that genes such as PSEN1 and PSEN2, which are responsible for early-onset Alzheimer disease, have also been implicated in dilated cardiomyopathy.

Most familial dilated cardiomyopathies are inherited in an autosomal dominant fashion. X-linked inheritance of dilated cardiomyopathy has been described in patients with mutations in the DMD gene (Duchenne muscular dystrophy) and the TAZ gene (Barth syndrome). Autosomal recessive inheritance has been described in mutations of the TNNI3 gene, which encodes troponin I.

Hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy is usually inherited in an autosomal dominant fashion with incomplete penetrance. Mutations in four genes that encode sarcomeric proteins—TNNT2, MYBPC3, MYH7, ­and TNNI3—account for approximately 90% of cases.[27] Most people with symptomatic hypertrophic cardiomyopathy will experience them at rest. Less often, a person with this disorder will experience an initial episode of VT or VF with significant exertion.

Arrhythmogenic right ventricular dysplasia

ARVD (also known as right ventricular cardiomyopathy) is characterized by replacement of the free wall of the right ventricle with fibrous tissue and the development of right ventricular hypertrophy. This disorder frequently results in sustained VT, which may degrade into VF.

The genetics of ARVD are extremely heterogeneous. More than 10 genes (eg, TGFB3, RYR2, DSP, PKP2, DSG2, DSC2,[28]  TMEM43, JUP[29] ) and seven additional loci (eg, 14q12-q22, 2q32.1-32.3, 10p14-p12, 10q22) have been implicated in the pathogenesis of this disorder, which is inherited in an autosomal dominant fashion with incomplete penetrance.[29] Those genes are believed to be responsible for approximately 40-50% of the total cases of ARVD.[28]

Brugada syndrome

Brugada syndrome is characterized by the specific ECG pattern of right bundle-branch block and ST-segment elevation in the early precordial leads, most commonly V1-V3, without any structural abnormality of the heart. It causes idiopathic VT or VF and carries a high risk for sudden cardiac death.[30]

Brugada syndrome can be caused by many genes. At least nine genes are known to cause Brugada syndrome (SCN5A, GPD1L, CACNA1C, CACNB2, SCN1B, KCNE3, SCN3B, HCN4, and KCND3), but SCN5A accounts for about 20% of cases, with other known "minor" genes comprising another 15% of cases.[31] Brugada syndrome is inherited in an autosomal dominant fashion.

Familial ventricular tachycardia

Familial VT is characterized by paroxysmal VT in the absence of cardiomyopathy or another identifiable electrophysiologic disorder. Familial VT is rare; investigation of families with paroxysmal VT will frequently reveal disorders such as Brugada syndrome, long QT syndrome, or catecholaminergic polymorphic VT. In at least one case, however, these disorders were ruled out, and the patient was found to have a somatic mutation in the GNAI2 gene.[32]

Ventricular tachycardia (VT) and coronary artery disease (CAD) are common throughout most of the developed world. In developing countries, VT and other heart diseases are relatively less common.

The incidence of VT in the United States is not well quantified, because of the clinical overlap of VT with ventricular fibrillation (VF), but examination of sudden death data provides a rough estimate of VT incidence. Most sudden cardiac deaths are caused by VT or VF,[1] at an estimated rate of approximately 300,000 deaths per year in the United States, or about half of the estimated cardiac mortality.[2]

A prospective surveillance study gave a sudden death incidence of 53 per 100,000 population, accounting for 5.6% of all mortality.[33] This is only a rough estimate of VT incidence, both because many patients have nonfatal VT and because arrhythmic sudden deaths may be associated with VF or bradycardia rather than with VT. In patients with ischemic cardiomyopathy and nonsustained VT, sudden death mortality approaches 30% in 2 years.

Morbidity from VT is associated with hemodynamic collapse. Resuscitated survivors may suffer ischemic encephalopathy, acute renal insufficiency, transient ventricular dysfunction, aspiration pneumonitis, and trauma related to resuscitative efforts.

Age-related demographics

VT is unusual in children but may occur in the postoperative cardiac setting or in patients with associated congenital heart disease. Tachydysrhythmias in children are more commonly due to paroxysmal supraventricular tachycardias (PSVTs).[34] The incidence of ischemic VT increases with age, regardless of sex, as the prevalence of CAD increases. VT rates peak in the middle decades of life, in concert with the incidence of structural heart disease. Idiopathic VT can be observed at any age.

Sex-related demographics

VT is observed more frequently in men because ischemic heart disease is more prevalent in men. Among patients with CAD in the Framingham Heart Study, male deaths were more common than female deaths (46% vs 34%, respectively).[35] It seems certain that as CAD becomes more common in women, the incidence of VT in women will increase.

Females with acquired or congenital long QT syndromes are at greater risk for sudden death. The opposite is true for arrhythmogenic right ventricular cardiomyopathy (a two-fold male predominance) and Brugada syndrome (an approximately eight-fold male predominance).

The prognosis in patients with ventricular tachycardia (VT) varies with the specific cardiac process, but it is predicted best by left ventricular function. Patients with VT may suffer heart failure and its attendant morbidity as a result of hemodynamic compromise. In patients with ischemic cardiomyopathy and nonsustained VT, sudden-death mortality approaches 30% in 2 years. In patients with idiopathic VT, the prognosis is excellent, with the major risk being injury incurred during syncopal spells.

Data from the Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction Trial suggest that VT or ventricular fibrillation occurring before coronary angiography and revascularization in the setting of ST-segment elevation myocardial infarction has a strong association with increased 3-year rates of death and stent thrombosis.[36]

Appropriate treatment can significantly improve the prognosis in selected patients. Beta-blocker therapy can reduce the risk of sudden cardiac death from VT, and implantable cardioverter-defibrillators can terminate malignant arrhythmias.[37]

The prognosis does not always correlate with left ventricular function. Patients with long QT syndrome, right ventricular dysplasia, or hypertrophic cardiomyopathy may be at increased risk for sudden death despite relatively well preserved left ventricular function. These possibilities should be considered in any patient with a strong family history of premature sudden death.

Ventricular tachycardia (VT) can be symptomatic. Symptoms of VT are often a function of the associated heart rate, or the causal process, such as an acute myocardial infarction (MI). Symptomatic patients typically present with palpitation, lightheadedness, and syncope from diminished cerebral perfusion. Chest pain may result from ischemia or from the rhythm itself. Understandably, patients often experience anxiety. Syncope is more common when VT occurs 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 occasional cannon A waves. Dyspnea may be related to increased pulmonary venous pressures and occasional left atrial contraction against a closed mitral valve.

VT may also be asymptomatic, or the symptoms may be those of the associated triggered therapy (eg, an implantable cardioverter-defibrillator [ICD] shock).

Eliciting a history of risk factors for VT is important. These include prior MI, 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. For athletes, determination of the risk for VT should be part of the preparticipation history and physical examination. 

Any patient with a strong family history of premature (ie, before age 40 years) sudden death should be evaluated for inherited arrhythmia syndromes, including the following:

• Long QT syndrome
• Short QT syndrome ^{[38, 39]}
• Brugada syndrome
• Arrhythmogenic right ventricular dysplasia
• Catecholaminergic polymorphic VT
• Hypertrophic cardiomyopathy

Aside from tachycardia, findings in patients with ventricular tachycardia (VT) generally reflect the degree of hemodynamic instability. Episodes of VT are often associated with hypotension and tachypnea. Signs of diminished perfusion may be present, including a 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 (S1) may vary in intensity as a result of loss of atrioventricular (AV) synchrony.

In patients who have converted to sinus rhythm (whether spontaneously or after cardioversion), relevant physical findings would be related to any underlying structural heart disease. These 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 heart failure is present. Sinus rhythm is often interrupted by ventricular extrasystole.

The following changes may be seen in the patient’s mental status:

• Anxiety
• Agitation
• Lethargy
• Coma

Electrocardiography (ECG) is the criterion standard for the diagnosis of ventricular tachycardia (VT).[9] In a patient who is hemodynamically unstable or unconscious, however, the diagnosis of VT is made from the physical findings and ECG rhythm strip only.

Advanced cardiac life support (ACLS) protocols should be quickly followed. Laboratory tests should be deferred until electrical cardioversion has restored sinus rhythm and the patient is stabilized. If the patient is hemodynamically stable at presentation, a 12-lead ECG and electrolyte levels may be obtained before attempted conversion with medications or direct current (DC) cardioversion. Note that if electrolyte levels are not obtained in an acute evaluation of VT post conversion, the hyperadrenergic state or hemodynamic compromise often associated with VT may affect the subsequently obtained electrolyte laboratory values.

The ECG should be repeated once sinus rhythm has been restored, or when prior VT is suspected, as in a patient who experienced syncope. The ECG may also provide clues for differentiating among potential arrhythmia mechanisms or causes of VT, such as the following:

• Acute or chronic infarction
• Ischemia
• Myocardial scar
• Ventricular preexcitation
• Hypertrophy
• Conduction disease
• QT prolongation
• Other precordial repolarization abnormalities (eg, Brugada syndrome, arrhythmogenic right ventricular dysplasia [ARVD])

Appropriate laboratory studies are indicated. In addition, a full 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 VT. These patients often require aggressive management of the underlying ischemic heart disease and heart failure.

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 includes the following recommendations[44] :

• Assessment of the risk for sudden death in patients with cardiomyopathies, particularly in those with hypertrophic cardiomyopathy, sarcoidosis, ARVD, or neuromuscular disease
• Evaluation for genetic arrhythmia syndromes in patients younger than 40 years with unexplained sudden cardiac death, unexplained near drowning, or recurrent syncope in the absence of ischemic or other structural heart disease
• Cardiac evaluation and genetic counseling and genetic testing as appropriated on the basis of clinical findings in first-degree relatives of victims of sudden cardiac death who were aged 40 years or younger

Screening of first-degree relatives should be contemplated when a patient is identified as having any of the following:

• Long QT syndrome
• Short QT syndrome
• Hypertrophic or dilated cardiomyopathy
• Right ventricular dysplasia

Family screening typically involves the following:

• History and physical examination
• ECG
• Echocardiography
• Treadmill testing

In some patients with spontaneous polymorphic VT, genetic studies may be helpful for family screening or for clarifying a diagnosis. Spontaneous polymorphic VT may be related to genetic mutations affecting ion channels, such as occur 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.

Chest radiography is indicated if symptoms suggest the possibility of heart failure or other cardiopulmonary pathology as a contributing factor. Cardiac computed tomography (CT) scanning and cardiac magnetic resonance imaging (cMRI) are evolving quickly but have not yet supplanted echocardiography and nuclear imaging for quantification of ventricular function. CMRI can be especially helpful in the evaluation of uncommon myocardial infiltrative diseases, such as sarcoidosis.

Assess electrolyte levels of all patients with ventricular tachycardia (VT), including serum potassium, magnesium, calcium, and phosphate levels. Ionized calcium levels are preferred to total serum calcium levels. Hypokalemia is a common VT trigger and is commonly seen in patients taking diuretics. Hypokalemia, hypomagnesemia, and hypocalcemia may predispose patients to either monomorphic VT or torsade de pointes.

In accordance with the clinical history, measure serum levels of therapeutic drugs (eg, digoxin, tricyclic antidepressants). Toxicology screens (eg, for methamphetamine, methadone, cocaine) may be helpful in cases related to recreational or therapeutic drug use.

Evaluate for myocardial ischemia or infarction with serum cardiac troponin I or T levels or other cardiac markers if symptoms or clinical signs of ischemia are present. Persistently elevated cardiac enzyme levels may also be an indication of ongoing myocarditis.

Polymorphic ventricular tachycardia

When the QRS complex varies from beat to beat, the rhythm is described as polymorphic ventricular tachycardia (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 meaning “twisting of the points” and refers to the unusual shifting-axis QRS complexes that appear as if the heart is rotating upon an axis.

Torsade de pointes typically occurs during sinus rhythm and in the presence of drugs or conditions that prolong the QT interval (eg, class IA antiarrhythmics, hypomagnesemia, droperidol). The dysrhythmia may occur either in the presence or in the absence of myocardial ischemia or infarction. The term torsade de pointes is reserved for polymorphic VT observed in the setting of a prolonged QT interval (see the images below). Other polymorphic VTs are occasionally observed during ischemia or myocarditis.

The typical initiation of torsade de points occurs with a “long-short” sequence—that is, a longer RR interval resulting in further prolongation of the QT interval, followed by an early depolarization occurring at a time of heterogeneous repolarization.

Torsade de pointes. Image A: This is polymorphic ventricular tachycardia associated with resting QT-interval prolongation. In this case, it was caused by the class III antiarrhythmic agent sotalol. This rhythm is also observed in families with mutations affecting certain cardiac ion channels. Image B: Torsade de pointes, a form of ventricular tachycardia. Courtesy of Science Source/BSIP.

This electrocardiogram reveals torsade de pointes.

Monomorphic ventricular tachycardia

When the ventricular activation sequence is constant, the electrocardiographic (ECG) pattern remains the same, and the rhythm is called monomorphic VT (see the image below). Monomorphic VT is most commonly seen in patients with underlying structural heart disease. There is typically a zone of slow conduction, most commonly the result of scarring or fibrillar disarray. Causes include prior infarct, any primary cardiomyopathy, surgical scar, hypertrophy, and muscle degeneration.

This tracing depicts monomorphic ventricular tachycardia.

Reentrant tachycardias occur when an electrical wavefront travels slowly through the zone of slow conduction (usually damaged muscle protected by scar tissue), 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.

Monomorphic VT is occasionally observed in patients with structurally normal hearts (idiopathic VT). These VTs are often exercise dependent, and their clinical behavior may be more consistent with triggered activity or abnormal automaticity.

Monomorphic VTs are typically named for their site of origin. The following are the most commonly involved sites[45] :

• Right ventricular outflow tract
• Left ventricular outflow tract
• Left ventricular septum
• Aortic root

The QRS morphology during VT can be used to predict the exit site from the zone of slow conduction[46] or the site of origin, regardless of the underlying substrate. The earliest activation is closest to the leads with QS complexes during tachycardia.[47]

Monomorphic VTs have classically been considered benign. Rarely, however, they may result in sudden death, despite the presence of a structurally normal heart.[48]

Differentiating monomorphic VT from supraventricular tachycardia

Polymorphic VT is easily diagnosed after exclusion of lead motion artifact. Monomorphic VT can be more difficult to sort out. The ECG will demonstrate a wide-complex tachycardia, representing either VT or supraventricular tachycardia (SVT) with aberrant conduction. If the patient is unstable, or if differentiation between VT and SVT is uncertain, treat the rhythm as VT; the majority of patients with wide-complex regular tachycardias will have VT. If the patient is stable, the ECG can be examined for clues to the mechanism underlying the arrhythmia.

Atrioventricular dissociation

AV dissociation (see the images below), is apparent in approximately half of VT episodes; when present, it is a hallmark of VT.[49]  AV dissociation occurs because the sinus node is depolarizing the atria at a rate that is slower than the pathologic, faster ventricular rate. At times, P waves can be seen in between or embedded in the QRS complexes, but the P waves and QRS complexes have their own independent rates.

The electrocardiogram shows a form of idiopathic ventricular tachycardia (VT) seen in the absence of structural heart disease. This rhythm arises from the left ventricular septum and often responds to verapamil. Upon superficial examination, it appears to be supraventricular tachycardia with bifascicular conduction block. Closer examination of lead V1 shows narrowing of fourth QRS complex, consistent with fusion between the wide QRS complex and the conducted atrial beat, confirming atrioventricular dissociation and a VT mechanism.

This tracing depicts atrioventricular dissociation.

Retrograde conduction can also exist from the ventricles to the atria via the AV node. This is not AV dissociation and reveals itself on ECG as a 1:1 correlation between the wide QRS complex and an inverted P wave, which follows the QRS complex.

Fusion and capture beats

Fusion beats and capture beats can occur in the presence of VT, depending on the refractory period of the AV node and on the timing of ventricular and atrial depolarizations, respectively (see the image below). If present, they help distinguish VT from SVT with aberrant conduction.

Fusion beats, capture beats, and atrioventricular dissociation can be seen on this electrocardiogram.

A fusion beat has a mixed morphology because of normal AV node/His-Purkinje conduction occurring simultaneously with abnormal ventricular depolarization. A normally conducted impulse travels from the AV node through the normal conduction pathway (producing a narrow QRS complex), and the competing impulse originates from the abnormal ectopic ventricular focus outside of the normal conduction pathway (producing a wide QRS complex). The two impulses converge, leading to a mixed (fused) QRS.

A capture beat occurs when an atrial impulse arrives at the AV node when the node has just recovered from its refractory period. The timing must be just right, because the AV node is frequently in its refractory state as a result of depolarization caused by retrograde conduction from the rapid ventricular rhythm. When this occurs, conduction proceeds normally through the AV node/His-Purkinje system, “capturing” the ventricle and leading to a normal, narrow QRS complex.

Unfortunately, most VT tracings do not show obvious clues of AV dissociation, fusion, or capture. In such cases, the QRS morphology may often (depending on the clinical context) provide enough information to permit an accurate diagnosis. The two most commonly applied sets of ECG criteria are described below.

Brugada et al proposed ECG discrimination criteria for VT that focused primarily on the QRS morphologies in the precordial leads (V1-V6).[15]  They reported a sensitivity of 98.7% and a specificity of 96.5% with the following criteria:

• Absence of RS complexes in the precordial leads
• RS duration exceeding 100 ms in any precordial lead
• Ventriculoatrial dissociation in any of 12 leads
• Certain QRS morphologies, such as QR or QS in lead V6

Vereckei et al refined a different ECG algorithm based on a single lead, aVR, and reported better accuracy than was achieved with the Brugada criteria.[16]  They noted the presence of a negative QRS complex in lead aVR during right or left bundle-branch conduction of SVTs. VT was predicted by the following:

• Presence of an initial R wave in lead aVR
• Width of an initial R or Q wave exceeding 40 ms in lead aVR
• Notching on the initial downstroke of a predominantly negative QRS complex in lead aVR
• A ventricular activation-velocity ratio (V _i/V _t) of 1 or less

Differentiating VT from sinus tachycardia

The image below demonstrates a tachycardia with a 1:1 atrial-to-ventricular ratio. It is not immediately clear whether the atria are driving the ventricles (sinus tachycardia) or the ventricles are driving the atria (VT).

This electrocardiogram is from a 32-year-old woman with recent-onset heart failure and syncope.

In this case, a diagnosis of sinus tachycardia would require the presence of severe conduction disease manifesting as marked first-degree AV block with left bundle-branch block. However, close inspection shows that the actual diagnosis is VT, as indicated by absence of RS complexes in the precordial leads, a QS pattern in lead V6, and an R wave in lead aVR. The patient proved to have an incessant VT associated with dilated cardiomyopathy.

Signal-averaged ECG

Signal-averaged ECG (SAECG) is a noninvasive test that often demonstrates abnormal results in patients with VT related to a prior infarct or right ventricular dysplasia. SAECG—along with heart rate variability (HRV), baroflex sensitivity, and heart rate turbulence—may be useful for refining the diagnosis and risk stratification of patients with ventricular arrhythmias or those who are at increased risk of developing life-threatening ventricular arrhythmias.[40]

Echocardiography is used for patients at high risk for serious ventricular arrhythmias or sudden cardiac death. In particular, echocardiography can provide an estimate of left ventricular (LV) systolic function, and the presence or absence of associated LV wall motion abnormalities commonly indicative of a prior scar. Echocardiography may also show findings suggestive of a myocardial infiltrative process. Imaging of the right ventricle (RV) may be more limited, and other imaging techniques may be required to obtain accurate and global views of RV function. The high-risk group consists of patients with any of the following[40] :

• Dilated, hypertrophic, or RV cardiomyopathy
• A history of acute myocardial infarction
• Inherited disorders associated with sudden cardiac death

Cardiac computed tomography (CT) scanning and cardiac magnetic resonance imaging (cMRI) are evolving quickly but have not yet supplanted echocardiographic and nuclear imaging for quantification of ventricular function. CMRI can be especially helpful in the evaluation of uncommon myocardial infiltrative diseases, such as sarcoidosis.

The use of late gadolinium enhancement (LGE) and extracellular volume (ECV) cMRI appear to have the potential to predict the estimated 5-year risk of sudden death and syncope or nonsustained ventricular tachycardia (VT) in patients with hypertrophic cardiomyopathy (HCM).[50]  In a study of 73 German patients with HCM and 16 control subjects, investigators found that not only was global ECV was the best predictor of an increased risk of sudden death but that when used in conjunction with the sudden cardiac risk score, the diagnostic accuracy to identify HCM patients with syncope or nonsustained VT was significantly improved. These findings may have implications for improved patient selection of HCM patients for ICD implantation.[50]

Although cMRI is often used for the 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 this disorder.

MRI, cardiac CT scanning, or radionuclide angiography can be useful in patients with ventricular arrhythmias when echocardiography fails to provide accurate evaluation of left or right ventricular function. These studies may also be useful for assessment of structural changes in the heart.[40]

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, and event recording. The goal is to document the patient’s rhythm during symptoms. Individuals with infrequent symptoms are best served by the implantation of a loop recorder, which may have a battery life of 2-4 years.

If such techniques are not practical, a provocative electrophysiologic study can be performed.

Genetic testing is now feasible for a variety of inherited disorders that may cause long QT syndrome, arrhythmogenic right ventricular dysplasia, or dilated or hypertrophic cardiomyopathy. However, the absence of a defined genomic mutation does not exclude these abnormalities, and interpretation of mutations, especially those resulting in a noncoding alteration is presently difficult. 

The current approach is not exhaustive and is focused on established monogenic germline abnormalities and tracking these abnormalities in a defined family.

The advent of cardiac magnetic resonance imaging (cMRI) has facilitated the diagnosis of infiltrative cardiomyopathies but, occasionally, myocardial biopsy with special histologic processing may be useful in the diagnosis of arrhythmogenic right ventricular dysplasia or a hypertrophic or infiltrative myopathy. Most reentrant ventricular tachycardias (VTs) are related to myocardial scarring from ischemic or dilated cardiomyopathy. Fibrotic replacement of myocytes and interweaving of scar tissue with functional myocytes is common along slow conduction zones of VT circuits.

The presence of a dual-chamber pacemaker or implantable cardioverter-defibrillator (ICD) can occasionally simplify the diagnosis. Most contemporary devices are capable of recording and logging tachyarrhythmias for subsequent analysis during interrogation of the implanted device, as well as providing real-time telemetry of intracardiac signals.

Analysis may reveal the disease process underlying the ventricular tachycardia (VT). However, the episode may prove to have been triggered by the device itself. Possibilities include the following:

• Tracking of an atrial tachyarrhythmia in a dual-mode, dual-pacing, dual-sensing (DDD) device or an atrial-triggered, ventricular-inhibited (VDD) device
• Endless loop tachycardia
• Inappropriate rate-responsive pacing due to sensor problems or incorrect sensor programming
• Overt pacemaker failure (runaway pacer)

The most common problem involves the patient whose device is tracking atrial fibrillation or atrial flutter. In the absence of a mode-switching algorithm, a DDD or VDD 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 are induced after conditioning pacing drives in an attempt to induce reentrant arrhythmia.[51]  The response of the arrhythmia to pharmacologic agents can be assessed (eg, beta adrenergic stimulation or blockage, adenosine, calcium blockers).

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. The diagnostic yield of EPS is highest in patients with reentrant VT circuits.

EPS is particularly relevant in patients considered 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 the diagnosis of right ventricular dysplasia is being considered, many laboratories perform right ventricular angiography at the time of the EPS. Diagnostic abnormalities include right ventricular dilatation, dyskinesis, and aneurysms.

EPS is recommended for diagnostic assessment of patients with a remote history of myocardial infarction and symptoms related to ventricular tachyarrhythmias, including palpitations, presyncope, and syncope, and in patients with coronary heart disease to guide and measure the efficacy of VT ablation. EPS is reasonable for diagnostic evaluation in patients with palpitations or suspected outflow tract VT.[40]

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.

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.

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.

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.

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.

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.

Advanced cardiac life support 

Updated cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) guidelines were issued in 2015 by the following organizations[60, 61, 62] :

• American Heart Association (AHA)
• European Resuscitation Council (ERC)
• The International Liaison Committee on Resuscitation (ILCOR)

The following summarizes the AHA adult cardiac arrest algorithm for ventricular fibrillation (VF) or pulseless ventricular tachycardia (pVT)[60] :

• Activate the emergency response system.
• Initiate cardiopulmonary resuscitation (CPR) and give oxygen when available.
• Verify the patient is in VF as soon as possible (ie, automated external defibrillator [AED] and quick look with paddles).
• Defibrillate once: Use a device specific recommendations (ie, 120-200 J for biphasic waveform; 360 J for monophasic waveform); if unknown, use the maximum available.
• Resume CPR immediately without pulse check and continue for 5 cycles. One cycle of CPR equals 30 compressions and 2 breaths; 5 cycles of CPR should take roughly 2 minutes (compression rate 100 per minute). Do not check for rhythm/pulse until 5 cycles of CPR are completed.
• During CPR, minimize interruptions while securing intravenous (IV) access and performing endotracheal intubation. Once the patient is intubated, continue CPR at 100 compressions per minute without pauses for respirations, and administer respirations at 10 breaths per minute.
• Check rhythm after 2 minutes of CPR.
• Repeat a single defibrillation if rhythm check still reveals VF/pVT. Selection of fixed versus escalating energy for subsequent shocks is based on the specific manufacturer’s instructions. For a manual defibrillator capable of escalating energies, higher energy for the second and subsequent shocks may be considered.
• Resume CPR for 2 minutes immediately after defibrillation.
• Continuously repeat the cycle of (1) rhythm check, (2) defibrillation, and (3) 2 minutes of CPR.
• Administer a vasopressor: Give a vasopressor during CPR before or after the shock when IV or intraosseous (IO) access is available. Administer epinephrine 1 mg every 3-5 minutes.
• Administer antidysrhythmics: Give antidysrhythmic agents during CPR before or after the shock. Administer amiodarone 300 mg IV/IO once; then, consider administering an additional 150 mg once.

In addition, correct the following if necessary and/or possible:

• Hypovolemia
• Hypoxia
• Hydrogen ion (acidosis): Consider bicarbonate therapy.
• Hyperkalemia/hypokalemia and metabolic disorders
• Hypoglycemia: Check fingerstick or administer glucose.
• Hypothermia: Check core rectal temperature.
• Toxins
• Tamponade, cardiac: Check with ultrasonography.
• Tension pneumothorax: Consider needle thoracostomy.
• Thrombosis, coronary or pulmonary: Consider thrombolytic therapy if suspected.
• Trauma

According to the AHA, if all the following factors are present, termination of resuscitation in out-of-hospital cardiac arrest (OHCA) may be considered[60] :

• Arrest was not witnessed by emergency medical services (EMS) personnel
• No return of spontaneous circulation (ROSC) prior to transport
• No AED shock delivered prior to transport

In addition, in intubated patients, failure to achieve an end-tidal carbon dioxide (ETCO2) over 10 mm Hg by waveform capnography after 20 minutes of CPR may be considered as one component of a multimodal approach to decide when to end resuscitative efforts. However, no studies of nonintubated patients have been reviewed and ETCO2 should not be used as an indication to end resuscitative efforts.

Defibrillation

AHA recommendations for defibrillation include the following[60] :

• Use defibrillators (using biphasic truncated exponential [BTE], rectilinear biphasic [RLB], or monophasic waveforms) to treat atrial and ventricular arrhythmias. (Class I)
• Defibrillators using biphasic waveforms (BTE or RLB) are preferred. (Class IIa)
• Use a single-shock strategy (as opposed to stacked shocks) for defibrillation. (Class IIa)
• The benefit is unclear for using a multimodal defibrillator in manual instead of automatic mode. (Class IIb)
• The value is unclear regarding VF waveform analysis to guide management of defibrillation. (Class IIb)

Overall, the ERC and ILCOR guidelines concur with those of the AHA,[61, 62]  but the ERC includes an additional recommendation for self-adhesive defibrillation pads which are preferred over manual paddles and should always be used when they are available.[62]

Adjuncts for airway control and ventilation

The AHA guidelines provide the following recommendations for airway control and ventilation[60, 81] :

• Advanced airway placement in cardiac arrest should not delay initial CPR and defibrillation for VF arrest. (Class I)
• If advanced airway placement will interrupt chest compressions, consider deferring insertion of the airway until the patient fails to respond to the initial CPR and defibrillation attempts or demonstrates ROSC. (Class IIb)
• The routine use of cricoid pressure in cardiac arrest is not recommended. (Class III)
• Either a bag-mask device or an advanced airway may be used for oxygenation and ventilation during CPR in both the in-hospital and out-of-hospital setting. (Class IIb) The choice of bag-mask device versus advanced airway insertion should be determined by the skill and experience of the provider.
• For healthcare providers trained in their use, either an supraglottic airway (SGA) device or an endotracheal tube (ETT) may be used as the initial advanced airway during CPR. (Class IIb)
• Providers who perform endotracheal intubation should undergo frequent retraining (Class I)
• To facilitate delivery of ventilations with a bag-mask device, oropharyngeal airways can be used in unconscious (unresponsive) patients with no cough or gag reflex and should be inserted only by trained personnel. (Class IIa)
• In the presence of known or suspected basal skull fracture or severe coagulopathy, an oral airway is preferred. (Class IIa)
• Continuous waveform capnography in addition to clinical assessment is the most reliable method of confirming and monitoring correct placement of an ETT. (Class I)
• If continuous waveform capnometry is not available, a nonwaveform CO ₂ detector, esophageal detector device, or ultrasonography used by an experienced operator is a reasonable alternative. (Class IIa)
• After placement of an advanced airway, it is reasonable for the provider to deliver 1 breath every 6 seconds (10 breaths/min) while continuous chest compressions are performed. (Class IIb)
• Automatic transport ventilators (ATVs) can be useful for ventilation of adult patients in noncardiac arrest who have an advanced airway in place in both out-of-hospital and in-hospital settings. (Class IIb)

There are no significant differences in the recommendations from the ERC or ILCOR.[61, 62]

Medication management

The 2015 AHA guidelines offers the following recommendations for the administration of drugs during cardiac arrest[60] :

• Amiodarone may be considered for VF or pVT that is unresponsive to CPR, defibrillation, and a vasopressor therapy; lidocaine may be considered as an alternative. (Class IIb)
• Routine use of magnesium for VF/pVT is not recommended in adult patients. (Class III)
• Inadequate evidence exists to support routine use of lidocaine. However, the initiation or continuation of lidocaine may be considered immediately after ROSC from cardiac arrest due to VF/pVT. (Class IIb)
• Inadequate evidence exists to support the routine use of a beta blocker after cardiac arrest. However, the initiation or continuation of a beta blocker may be considered after hospitalization from cardiac arrest due to VF/pVT. (Class IIb)
• Atropine during pulseless electrical activity (PEA) or asystole is unlikely to have a therapeutic benefit. (Class IIb)
• There is insufficient evidence for or against the routine initiation or continuation of other antiarrhythmic medications after ROSC from cardiac arrest.
• Standard-dose epinephrine (1 mg every 3-5 minutes) may be reasonable for patients in cardiac arrest. (Class IIb); high-dose epinephrine is not recommended for routine use in cardiac arrest. (Class III)
• It may be reasonable to administer epinephrine as soon as feasible after the onset of cardiac arrest due to an initial nonshockable rhythm. (Class IIb)
• Vasopressin has been removed from the adult cardiac arrest algorithm as it offers no advantage in combination with epinephrine nor as a substitute for standard-dose epinephrine. (Class IIb for both)

Evaluation 

Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death were published jointly in 2006 by the American College of Cardiology (ACC), the American Heart Association (AHA), and the European Society of Cardiology (ESC).[40]  In 2015, the European Society of Cardiology (ESC) released an updated guideline.[82]

The guidelines recommend assessment of family members of victims of sudden unexplained death syndrome (SUDS) or sudden arrhythmic death syndrome (SADS). Recommendations for the evaluation of suspected or known ventricular arrhythmias are summarized in the table below.[82]  

Table 1. Evaluation of Suspected or Known Ventricular Arrhythmias (Open Table in a new window)

Medical management

The 2015 ESC guidelines note that the selection of appropriate therapy is focused on the associated medical conditions that may contribute to and/or exacerbate the arrhythmia, the risk posed by the arrhythmia, and the risk–benefit aspects of potential therapy.[82]  Management involves appropriate antiarrhythmic therapy with drugs, implantable devices, ablation, or surgery. Beta blockers are recommended as the first line of treatment for management of ventricular arrhythmias and prevention of sudden cardiac death.[82]

Implantable cardioverter-defibrillator therapy

A 2013 published report of the American College of Cardiology Foundation, Heart Rhythm Society, American Heart Association, American Society of Echocardiography, Heart Failure Society of America, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance (ACCF/HRS/AHA/ASE/HFSA/SCAI/SCCT/SCMR) provided the following appropriate use criteria for implantable cardioverter-defibrillator (ICD) therapy.[4]  

ICD therapy is used for secondary prevention in the following groups[4] : 

• Most patients with hemodynamically unstable ventricular tachycardia (VT)
• Most patients with prior myocardial infarction (MI) and hemodynamically stable sustained VT
• Most cardiomyopathy patients with unexplained syncop
• Most patients with genetic sudden death syndromes when unexplained syncope is noted

The 2015 ESC guidelines include the following recommendations for ICD for secondary prevention[82] :

• Patients hemodynamically unstable VT in the absence of reversible causes or within 48 hours after an MI who are receiving chronic optimal medical therapy and have a reasonable expectation of survival longer than1 year. (Class I)
• Patients with recurrent sustained VT (not within 48 hours after an MI) who are receiving chronic optimal medical therapy, have a normal left ventricular ejection fraction (LVEF) and have a reasonable expectation of survival with good functional status for longer than 1 year. (Class IIa)
• Amiodarone may be considered when an ICD is not available, is contraindicated for concurrent medical reasons, or is refused by the patient. (Class IIb)

Wearable cardioverter-defibrillator therapy

The 2016 AHA recommendations for wearable cardioverter-defibrillator (WCD) therapy are summarized below[83] :

• A WCD is reasonable when there is a clear indication for an implanted/permanent device accompanied by a transient contraindication or interruption in ICD care (ie, infection). (Class IIa)
• A WCD is reasonable as a bridge to more definitive therapy, such as cardiac transplantation. (Class IIa)
• A WCD may be reasonable when there is concern about a heightened risk of sudden cardiac death (SCD) that may resolve over time or with treatment of LV dysfunction. (Class IIb) 
• A WCD may be appropriate as bridging therapy in situations associated with an increased risk of death in which ICDs have been shown to reduce SCD but not overall survival. (Class IIb) 
• A WCD should not be used when the nonarrhythmic risk is expected to significantly exceed the arrhythmic risk, particularly in patients who are not expected to survive longer than 6 months. (Class III)

In its 2013 expert consensus statement on inherited primary arrhythmia syndromes, the Heart Rhythm Society/European Heart Rhythm Association/Asia Pacific Heart Rhythm Society (HRS/EHRA/APHRS) indicated catecholaminergic polymorphic ventricular tachycardia (CPVT) can be diagnosed when any for the following criteria are met[84] :

• Structurally normal heart, normal electrocardiogram (ECG), and unexplained exercise or catecholamine-induced bidirectional VT or polymorphic ventricular premature beats (VPBs) or VT in an individual younger than 40 years
• Presence of a pathogenic mutation
• Family history of CPVT with a normal heart, exercise-induced premature ventricular contractions or bidirectional/polymorphic VT
• Structurally normal heart and coronary arteries, normal ECG, and unexplained exercise or catecholamine-induced bidirectional VT or polymorphic VPBs or VT in an individual older than 40 years

Management recommendations include[84] :

Class I

• Limit or avoid competitive sports, strenuous exercise, and/or stressful environments
• Beta blockers for all symptomatic patients
• Placement of an implantable cardioverter-defibrillator for patients who experience cardiac arrest, recurrent syncope, or polymorphic/bidirectional VT despite optimal medical management, and/or left cardiac sympathetic denervation (LCSD)

Class IIa

• Flecainide in addition to beta blockers in patients who experience recurrent syncope or polymorphic/bidirectional VT while on beta blockers
• Beta blockers for carriers of a pathogenic CPVT mutation without clinical manifestations (concealed mutation-positive patients).

Class IIb

• Consider LCSD in patients who experience recurrent syncope or polymorphic/bidirectional VT/several appropriate ICD shocks while on beta blockers and in patients for whom beta blockers are contraindicated.

Class III

• ICD is not indicated as a stand-alone therapy in an asymptomatic CPVT patients. 
• Programmed electrical stimulation is not indicated.

In general, the 2015 ESC guidelines concur with the recommendations above as well as include the following additional guidance[82] :

• Flecainide should be considered in addition to beta blockers in patients with an ICD to reduce appropriate ICD shocks. (Class IIa)

The mainstays of treatment for clinically stable ventricular tachycardia (VT) are the various antiarrhythmic drugs. In the United Sates, the intravenous (IV) antiarrhythmic drugs available for suppression of acute monomorphic VT are limited to procainamide, lidocaine, and amiodarone, along with the beta-adrenergic blocking agents metoprolol, esmolol, and propranolol. Bretylium is no longer available.

In view of the relatively narrow therapeutic windows with these agents, careful attention must be paid to drug pharmacokinetics. Most antiarrhythmic drugs may actually cause ventricular arrhythmias, and risks generally increase with rising serum drug levels.

IV administration of antiarrhythmics is used for the suppression of acute VT. These agents alter the electrophysiologic mechanisms that are responsible for the arrhythmia. Amiodarone is the drug of choice for acute VT refractory to cardioversion shock. After recovery, oral medications are used for long-term suppression of recurrent VT. Current evidence favors class III antiarrhythmic drugs over class I drugs.

Class Summary

Class IA antiarrhythmics increase the refractory periods of the atria and ventricles. Myocardial excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity.

Procainamide (Procanbid, Pronestyl, Pronestyl [SR])

Procainamide is a class IA antiarrhythmic used for VT that is refractory to defibrillation and epinephrine. It is indicated for ventricular arrhythmias such as sustained VT. Procainamide is available only in IV form and is rarely used, because of hypotension and proarrhythmia risk. However, procainamide still maintains a specific niche as the drug of choice for management of stable preexcited atrial fibrillation. Its use is contraindicated by the presence of QT prolongation or congestive heart failure.

Quinidine (Quinidex, Quinora, Quinalan, Cardioquin)

Quinidine is a class IA antiarrhythmic that depresses myocardial excitability and conduction velocity. It is indicated for sustained VT but is rarely used, because of proarrhythmia risk. It still maintains a specific niche for VT suppression in specific patients with Brugada syndrome.

Class Summary

Class IB antiarrhythmics suppress automaticity of conduction tissue by increasing the electrical stimulation threshold of the ventricle and His-Purkinje system and inhibiting spontaneous depolarization of the ventricles during diastole through a direct action on the tissues. These antiarrhythmics block both initiation and conduction of nerve impulses by decreasing the neuronal membrane’s permeability to sodium ions, thereby inhibiting depolarization, with resultant blockade of conduction.

Lidocaine (Xylocaine, Nervocaine, LidoPen, Duo-Trach)

Lidocaine is an IV class IB antiarrhythmic that increases the electrical stimulation threshold of the ventricle, suppressing the automaticity of conduction through the tissue. Although lidocaine may terminate VT successfully, it may increase the overall mortality in peri-infarction VT. It can only be given IV. Its use for VT has declined as a consequence of trials showing IV amiodarone to be superior.

Mexiletine (Mexitil)

Mexiletine is a class IB antiarrhythmic that is indicated for ventricular arrhythmias such as sustained VT. It is a sodium-channel blocker and the closest oral analogue to lidocaine. Mexiletine is generally well tolerated and is occasionally used in patients with VT who respond to IV lidocaine. Class IB sodium channel–blocking drugs are generally felt to be safer than IC drugs, but no large comparative trials exist. This drug is still occasionally used for outpatient VT suppression.

Class Summary

Class IC antiarrhythmics slow conduction in cardiac tissue by altering the transport of ion across membranes, thus causing slight prolongation of refractory periods and decreasing the rate of rise of action potential without affecting its duration. These agents are typically avoided in the presence of coronary artery disease.

Flecainide (Tambocor)

Flecainide is a class IC antiarrhythmic approved for treatment of life-threatening ventricular arrhythmias. It blocks sodium channels, producing a dose-related decrease in intracardiac conduction in all parts of the heart, with the greatest effect on the His-Purkinje system (HV conduction). The effects of flecainide on atrioventricular (AV) nodal conduction time and intra-atrial conduction times, though present, are less pronounced than are the drug's effects on ventricular conduction velocity.

Flecainide carries a US Food and Drug Administration (FDA) black box warning regarding increased mortality when the drug is used in ischemic cardiomyopathy patients. Consequently, the use of flecainide is avoided in patients with structural heart disease. This drug is used almost exclusively for suppression of atrial arrhythmias in the structurally normal heart.

Propafenone (Rythmol)

Propafenone is similar in function to flecainide and carries a similar black box warning. It is almost exclusively used for suppression of atrial arrhythmias in the structurally normal heart.

Class Summary

Class III antiarrhythmics prolong the action potential duration. Some agents in this class inhibit adrenergic stimulation (alpha- and beta-blocking properties); affect sodium, potassium, and calcium channels; and prolong the action potential and refractory period in myocardial tissue. These effects result in decreased AV conduction and sinus node function.

Amiodarone (Cordarone, Pacerone, Nexterone)

Amiodarone is the drug of choice for the treatment of hemodynamically unstable VT that is refractory to other antiarrhythmic agents. Prehospital studies currently suggest that amiodarone is safe and efficacious for use in out-of-hospital cardiac arrest.

Sotalol (Betapace)

Sotalol is a class III antiarrhythmic that is primarily a potassium channel (IKr)-blocking drug with a weak beta-blocking effect. It is indicated for ventricular arrhythmias such as sustained VT. Because sotalol is renally cleared, renal function must be monitored.

Class Summary

At low doses, cardioselective beta blockers block response to beta1-adrenergic stimulation and have little or no effect on beta2 receptors.

Metoprolol (Lopressor, Toprol XL)

Metoprolol is a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions. During IV administration, carefully monitor the patient's blood pressure, heart rate, and electrocardiograms (ECGs). Long-term use of metoprolol has been shown to reduce

Class Summary

Electrolytes are considered therapeutic alternatives for refractory VT. Patients with persistent or recurrent VT after administration of antiarrhythmic drugs should be assessed for underlying electrolyte abnormalities as a cause of their refractory dysrhythmia. Electrolyte abnormalities that may be associated with VF include hyperkalemia, hypokalemia, and hypomagnesemia.

Magnesium sulfate, calcium chloride, and sodium bicarbonate are used in VT secondary to other medications. Magnesium sulfate acts as an antiarrhythmic agent. Sodium bicarbonate is used as an alkalinizing agent, and calcium chloride is used to treat VT caused by hyperkalemia.

Magnesium sulfate (MgSO4)

Magnesium sulfate is the agent of choice for torsades de pointes. It also may be useful for treating conventional VT, especially in patients with confirmed hypomagnesemia. Patients treated with magnesium sulfate require monitoring for hypermagnesemia; an overdose can cause cardiorespiratory collapse and paralysis.

Calcium chloride

Calcium chloride is useful for the treatment of hyperkalemia, hypocalcemia, or calcium-channel blocker toxicity. It moderates nerve and muscle performance by regulating the action potential excitation threshold.

Class Summary

Alkalinizing agents act as a buffer against acidosis by raising blood pH.

Sodium bicarbonate

Sodium bicarbonate is used only when the patient is diagnosed with bicarbonate-responsive acidosis (with pH ≤7.0), hyperkalemia, or a tricyclic antidepressant or phenobarbital overdose. Routine use of sodium bicarbonate is not recommended.

Class Summary

Alpha-/beta-adrenergic agents augment the coronary and cerebral blood flow that is present during the low-flow state associated with hemodynamic compromise from VT.

Epinephrine (Adrenalin)

Epinephrine is considered to be the single most useful drug in cardiac arrest, although it has never been shown to enhance long-term survival or functional recovery. Epinephrine stimulates alpha, beta1, and beta2 receptors, resulting in relaxation of smooth muscle, cardiac stimulation, and dilation of muscle vasculature.

Class Summary

Vasopressin is a vasoconstrictor without inotropic or chronotropic effects.

Vasopressin (ADH, Pitressin)

Vasopressin may improve vital organ blood flow, cerebral oxygen delivery, resuscitability, and neurologic recovery.