Ventricular Tachycardia

Introduction
Background

Ventricular tachycardia (VT) refers to any rhythm faster than 100 beats per minute arising distal from the bundle of His. The rhythm may arise from working ventricular myocardium and/or the distal conduction system. VT may cause important symptoms such as syncope, palpitations, and dyspnea. With a few exceptions, VT is associated with increased risk of sudden death. The most common setting for VT is ischemic heart disease, in which myocardial scar is the substrate for electrical reentry. It is often, but not always, associated with hemodynamic compromise, particularly if the left ventricle is impaired or the heart rate is especially fast. When sustained VT causes signs or symptoms of diminished perfusion, emergent treatment is necessary.

VT is distinguished from ventricular fibrillation (VF), which is a grossly disorganized rapid ventricular rhythm that varies in both interval and waveform. VF may be difficult to distinguish from rapid polymorphic VT. Sudden death accounts for approximately half of all deaths from cardiovascular disease and is generally caused by VT and VF.

There is a slight overlap with accelerated idioventricular rhythm when an automatic VT is noted from 100-120 beats per minute.

Pathophysiology

Ventricular tachycardia (VT) is a general term that includes any rapid rhythm, faster than 100-120 beats per minute, arising in the ventricle. Regardless of the arrhythmia mechanism, the severity of clinical symptoms determines the urgency with which VT must be treated. During VT, cardiac output is reduced due to the rapid heart rate and lack of a properly timed or coordinated atrial contraction. Ischemia and mitral1 insufficiency may also contribute to hemodynamic intolerance. Hemodynamic collapse is more likely when underlying left ventricular dysfunction is present or with very rapid rates. Diminished cardiac output may result in diminished myocardial perfusion, worsening inotropic response, and degeneration to VF, resulting in sudden death.

Monomorphic ventricular tachycardia

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


Monomorphic ventricular tachycardia.


Monomorphic VT is most commonly seen in patients with underlying structural heart disease. There is typically a zone of slow conduction, most commonly due to scarring and/or fibrillar disarray. Causes include prior infarct, any primary cardiomyopathy, surgical scar, hypertrophy, and muscle degeneration. Reentrant tachycardias occur when an electrical wavefront travels slowly through the zone of slow conduction (usually damaged muscle protected by scar), allowing the rest of the circuit time to repolarize. The wavefront breaks out of the scar, activates the ventricle, and reenters the slow conduction zone. The QRS morphology during VT can be used to predict the exit site from the zone of slow conduction.2

Although most patients with VT have underlying structural heart abnormalities, monomorphic VT is occasionally observed in patients with structurally normal hearts. The clinical behavior of these VTs may be more consistent with triggered activity or abnormal automaticity. Monomorphic VTs are typically named for their site of origin. The most commonly involved sites are the RV outflow tract, LV outflow tract, LV septum, and the aortic root.3 Although these arrhythmias have classically been considered benign, sudden death may occasionally be seen, despite the presence of a structurally normal heart.4
Polymorphic ventricular tachycardia

Polymorphic VT occurs when the ventricular activation sequence varies. It can be observed with or without structural heart disease. When polymorphic VT is observed in the setting of a prolonged resting QT electrocardiographic interval, it is termed torsade de pointes (torsades). Causes include certain drugs5 and inherited defects in cardiac ion channel structure or expression. Most of the causative drugs block the delayed rectifier cardiac potassium current, IKr and include quinidine, erythromycin, haloperidol, and many others (see updated list).


Polymorphic ventricular tachycardia.


Polymorphic VT and torsades are also observed in drug-free, structurally normal hearts when patients have genetic abnormalities affecting performance or intracellular processing of cardiac ion channels.6,7 Examples include long QT syndrome, short QT syndrome,8 Brugada syndrome,9 idiopathic ventricular fibrillation, and familial catecholaminergic polymorphic VT.10

Inherited long QT syndrome is most commonly caused by mutations affecting the function or expression of the cardiac potassium channels IKr and IKs. Loss of channel activity results in delayed repolarization, measured as a prolonged QT interval on the electrocardiogram. Occasionally, disease is associated with errors in intracellular processing of the same channels. Interestingly, gain of function potassium channel mutations have been implicated in sudden death related to abnormally short QT intervals.7

Studies of other families with polymorphic VT have implicated the cardiac sodium channel (Brugada syndrome, some long QT syndromes), membrane calcium channels (Timothy syndrome), cardiac sarcoplasmic reticular calcium channels (familial adrenergic polymorphic VT, one form of arrhythmogenic right ventricular cardiomyopathy/dysplasia), and IK1 (Anderson-Tawil syndrome).

When polymorphic VT is observed in the absence of a cardiac channel defect, the most common causes are ischemia and myocarditis.

Frequency
United States

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

International

The incidence of ventricular tachycardia (VT) in developed countries is thought to be similar to that of the United States. In other regions, VT incidence correlates with the prevalence of coronary artery disease.

Occasional pockets of unusual heart disease cause a locally increased risk of VT. Examples include the Greek island of Naxos (right ventricular dysplasia),12 parts of South America (Chagas disease),13 and northeastern Thailand (idiopathic VF).14

Mortality/Morbidity

In patients with monomorphic ventricular tachycardia (VT), mortality risk correlates with the degree of structural heart disease. Underlying structural heart diseases, such as ischemic cardiomyopathy, dilated cardiomyopathy, hypertrophic cardiomyopathy, Chagas disease, and right ventricular dysplasia, have all been associated with monomorphic or polymorphic VT degenerating to ventricular fibrillation.

If VT is associated with hemodynamic collapse, morbidity in resuscitated survivors can include ischemic encephalopathy, acute renal insufficiency, transient ventricular dysfunction, aspiration pneumonitis, and trauma related to resuscitative efforts.

If VT is hemodynamically tolerated, the incessant tachyarrhythmia may also cause a dilated cardiomyopathy. This may develop over a period of several months and resolves with successful management of the VT.15 A similar course is occasionally seen with ventricular bigeminy, despite the absence of sustained high rates.

Race

Ventricular tachycardia risk within populations generally varies with the risk factors for atherosclerosis, rather than ethnic differences per se.

Certain genetic groups carry genetically mediated risk of unusual heart disease. Examples include the Veneto region of Italy and Greek island of Naxos (right ventricular dysplasia),12 and northeastern Thailand (idiopathic ventricular fibrillation/Brugada syndrome)14 .
Sex

Ventricular tachycardia (VT) is observed more frequently in men because ischemic heart disease is more prevalent among men. Among patients with coronary artery disease in the Framingham study (see Framingham Heart Study), male deaths were more common than female deaths (46% vs 34%).16

Females with acquired or congenital long QT syndromes are at greater risk for sudden death. The opposite is true for arrhythmogenic right ventricular dysplasia (2-fold male predominance, and Brugada syndrome (~8-fold male predominance).

Age

The incidence of ischemic ventricular tachycardia (VT) increases with age, regardless of sex, as the prevalence of coronary artery disease increases.

Among patients younger than 35 years, the most common causes of sudden death, and presumably of VT, include hypertrophic cardiomyopathy, right ventricular cardiomyopathy, myocarditis, and long QT syndrome. Idiopathic VT can be observed at any age.
Clinical
History

Sustained ventricular tachycardia (VT) may precede a significant hemodynamic collapse. When this rhythm is present, it should be addressed rapidly.

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

Physical

During ventricular tachycardia (VT)

Physical findings during VT include tachycardia, which is often associated with hypotension and tachypnea.
Signs of diminished perfusion may be present, including diminished level of consciousness, pallor, and diaphoresis.
Jugular venous pressure may be high, and cannon a waves may be observed if the atria are in sinus rhythm.
The first heart sound may vary in intensity due to loss of AV synchrony.

During sinus rhythm following conversion
Physical findings during normal rhythm are related to any underlying structural heart disease. These may include and may include displacement of the point of maximal impulse (PMI), murmurs related to valvular heart disease or hypertrophic cardiomyopathy, and an S3 gallop.
Rales may be present during sinus rhythm if uncompensated congestive heart failure is present.
Sinus rhythm is often interrupted by ventricular extrasystoles.
Causes

Coronary artery disease is the most common cause of ventricular tachycardia (VT).

Reentrant circuits may form and typically include the border zone between electrically inactive scar tissue and electrically active myocardial tissue. Paradoxically, the slower electrical conduction within such border zones predisposes to the development of fast reentrant arrhythmia circuits.
In developed countries, coronary artery disease is the most common cause of myocardial scar. The substrate for electrical reentry (VT) may occur with any process that creates myocardial scar tissue, including the dilated cardiomyopathies, hypertrophic cardiomyopathy, right ventricular dysplasia, Chagas disease, and surgical incisions in the ventricle.
As noted in the Pathophysiology section, VT is classified according to its electrocardiographic appearance.

Monomorphic ventricular tachycardia
When the same QRS electrocardiographic wave repeats itself, the VT is considered monomorphic. This implies a repetitive, identical activation sequence in the ventricle.
Monomorphic VT is most commonly due to repetitive activation of the same reentrant ventricular myocardial circuit.
Occasionally, monomorphic VT is related to repetitive automatic beats arising from the same ectopic focus.

Polymorphic ventricular tachycardia
When the QRS complex varies from beat to beat, the rhythm is described as polymorphic VT and suggests a variable electrical activation sequence. The most notorious, and probably the most common, form of polymorphic VT is torsade de pointes, a French term suggesting a "twisting of the points" of the QRS complexes over time. This term is now reserved for polymorphic VT observed in the setting of a prolonged QT interval. Other polymorphic VTs are occasionally observed during ischemia or myocarditis.
Acquired QT prolongation is observed with certain potassium channel blocking medications. Most of the causative drugs block the delayed rectifier cardiac potassium current, IKr, and include quinidine, erythromycin, haloperidol, and many others. (See Drugs that Prolong the QT Interval and/or Induce Torsades de Pointes Ventricular Arrhythmia.)
Congenital long QT syndrome is a group of genetic disorders involving abnormal cardiac ion channels, (most commonly potassium channels responsible for ventricular repolarization).
In both acquired and congenital long QT syndromes, prolonged repolarization predisposes to torsade de pointes, which is most likely a reentrant rhythm with a constantly varying circuit. Other inherited ion channel abnormalities may cause idiopathic VF and familial polymorphic VT in the absence of QT prolongation.
In some patients, monomorphic VT occurs in the absence of structural heart disease (idiopathic VT).
These VTs are named according to their sites of origin, are often exercise dependent, and most often arise from the right and left ventricular outflow tracts and the left ventricular septum. The QRS morphology during tachycardia can be used to predict the VT site (see Images for examples).
Clinical behavior is generally consistent with an automatic, rather than reentrant, mechanism of origin. This becomes a critical point when treatment is considered. Although idiopathic VTs often respond to verapamil, this agent may cause hemodynamic collapse and death when administered to VT in patients with left ventricular dysfunction.
Triggers of VT include electrolyte abnormalities, ischemia, inflammation, and sleep apnea.
Hypokalemia is the most important arrhythmia trigger clinically, followed by hypomagnesemia. Hyperkalemia may also predispose to VT and VF, particularly in patients with structural heart disease.
Occasionally, VT is triggered by aggressive adrenergic stimulation, as is observed with cocaine use.

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