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Ventricular Tachycardia

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

Practice Essentials

Ventricular tachycardia (VT) or ventricular fibrillation (VF) causes most of the sudden cardiac deaths in the United States, at an estimated rate of approximately 300,000 deaths per year. VT refers to any rhythm faster than 100 (or 120) beats/min, with 3 or more irregular beats in a row, arising distal to the bundle of His. The rhythm may arise from working ventricular myocardium, the distal conduction system, or both. See the image below.

ECG shows rapid monomorphic ventricular tachycardi ECG shows rapid monomorphic ventricular tachycardia (VT), 280 beats/min, associated with hemodynamic collapse. Tracing was obtained from patient with severe ischemic cardiomyopathy during electrophysiologic study. Single external shock subsequently converted VT to sinus rhythm. Patient had 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, ventricular rate is simply too fast for P waves to be observed. VT at 240-300 beats/min is often termed ventricular flutter.

Signs and symptoms

History

Symptoms of VT include the following:

  • Palpitation
  • Light-headedness
  • Syncope
  • Chest pain
  • Anxiety

Physical examination

During VT, the following may be observed:

  • Hypotension
  • Tachypnea
  • Signs of diminished perfusion, including a diminished level of consciousness, pallor, and diaphoresis
  • High jugular venous pressure
  • Cannon a waves (if the atria are in sinus rhythm)
  • Variation in intensity of first heart sound, caused by loss of atrioventricular (AV) synchrony

After conversion, physical findings during normal sinus rhythm are related to any underlying structural heart disease.

VT can also result in sudden death. Patients in whom this occurs may first present with syncope.

See Clinical Presentation for more detail.

Diagnosis

Electrocardiography (ECG) is the criterion standard for the diagnosis of VT. If the clinical situation permits, a 12-lead ECG should be obtained before conversion of the rhythm. 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 cardiovascular 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.

Assess levels of serum electrolytes, including the following, in all patients with VT:

  • Calcium (ionized calcium levels are preferred to total serum calcium levels)
  • Magnesium
  • Phosphate

Hypokalemia, hypomagnesemia, and hypocalcemia may predispose patients to either monomorphic VT or torsades de pointes.

Laboratory studies can also include the following:

  • levels of therapeutic drugs (eg, digoxin)
  • Toxicology screens (potentially helpful in cases related to recreational drug use)
  • Serum cardiac troponin I or T levels or other cardiac markers (to evaluate for myocardial ischemia or infarction)

VT post conversion

In patients with VT post conversion, diagnosis proceeds as follows:

  • Repeat the ECG after termination of VT
  • Include electrolyte levels in an acute evaluation
  • Perform toxicology screens for cocaine metabolites and tricyclic antidepressants, in accordance with the patient’s clinical history
  • Check cardiac enzyme levels if clinical symptoms or signs of ischemia are present
  • Perform echocardiography and coronary angiography after conversion to sinus rhythm to assess for structural and ischemic heart disease

Electrophysiologic study

Diagnostic electrophysiologic study (EPS) requires placement of electrode catheters in the ventricle, followed by programmed ventricular stimulation using progressive pacing protocols. EPS is particularly relevant in patients considered to be at high risk for sudden death as a result of significant underlying structural heart disease.

See Workup for more detail.

Management

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). Unstable polymorphic VT is treated with immediate defibrillation.

Medications

  • In stable patients with monomorphic VT and normal left ventricular function, restoration of sinus rhythm is typically achieved with intravenous (IV) procainamide or sotalol
  • IV lidocaine is effective at suppressing peri-infarction VT but may increase the overall mortality risk
  • In torsades de pointes, magnesium sulfate may be effective if a long QT interval is present at baseline
  • For long-term treatment of most patients with left ventricular dysfunction, current clinical practice favors class III antiarrhythmics (eg, amiodarone and sotalol)
  • In patients with heart failure, the best proven antiarrhythmic drug strategies include the use of beta receptor–blocking drugs (eg, carvedilol, metoprolol, and bisoprolol); angiotensin-converting enzyme (ACE) inhibitors; and aldosterone antagonists

Implantable cardioverter-defibrillators

Multisociety guidelines recommend implantable cardioverter-defibrillator (ICD) therapy to augment medical management for the following[1] :

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

Ablation

Radiofrequency ablation (RFA) via endocardial or epicardial catheter placement can be used to treat VT in patients who have the following:

  • Left ventricular dysfunction from prior MI
  • Cardiomyopathy
  • Bundle-branch reentry
  • Various forms of idiopathic VT

See Treatment and Medication for more detail.

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Background

Ventricular tachycardia (VT) refers to any rhythm faster than 100 (or 120) beats/min arising distal to the bundle of His. The rhythm may arise from 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 2 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.

ECG shows rapid monomorphic ventricular tachycardi ECG shows rapid monomorphic ventricular tachycardia (VT), 280 beats/min, associated with hemodynamic collapse. Tracing was obtained from patient with severe ischemic cardiomyopathy during electrophysiologic study. Single external shock subsequently converted VT to sinus rhythm. Patient had 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, ventricular rate is simply too fast for P waves to be observed. VT at 240-300 beats/min is often termed ventricular flutter.
ECG shows slow monomorphic ventricular tachycardia ECG shows slow monomorphic ventricular tachycardia (VT), 121 beats/min, from patient with old inferior wall myocardial infarction and well-preserved left ventricular (LV) function (ejection fraction, 55%). Patient presented with symptoms of palpitation and neck fullness. Note ventriculoatrial dissociation, most obvious in V2 and V3. Slower VT rates and preserved LV function are associated with better long-term prognosis.
Polymorphic ventricular tachycardia. Polymorphic ventricular tachycardia.

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 myocardial scar, such as the following (see Etiology):

  • Dilated cardiomyopathy
  • Hypertrophic cardiomyopathy
  • Arrhythmogenic right ventricular dysplasia (ARVD) or cardiomyopathy
  • Chagas disease [2]
  • 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.[3]

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

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

ECG diagnosis of VT is generally straightforward but 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[4] and the Vereckei criteria[5] ) 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 Center, as well as Heart Rhythm Disorders, Supraventricular Tachycardia, and Palpitations.

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Pathophysiology

At the cellular level, 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 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. Torsades de pointes, seen in the long QT syndromes, is likely a combination of triggered activity and ventricular reentry.[6]

During VT, cardiac output is reduced as a consequence of decreased ventricular filling from the rapid heart rate and lack of properly timed or coordinated atrial contraction. Ischemia and mitral insufficiency[7] 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.[2] 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.[8] A similar course is occasionally seen in patients with frequent premature ventricular contractions or ventricular bigeminy, despite the absence of sustained high rates.[9]

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Etiology

Causes of VT include the following[3] :

  • Ischemic heart disease (most common)
  • Structural heart disease with disruption of normal conduction patterns (eg, nonischemic cardiomyopathy, ARVD or cardiomyopathy, and 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, and many others); drugs that slow myocardial conduction (eg, flecainide, propafenone, and 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, and hypomagnesemia
  • Sympathomimetic agents, including 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, and rheumatoid arthritis)

Hypokalemia is an important arrhythmia trigger, followed by hypomagnesemia. Hyperkalemia may also predispose to VT and 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 torsades de pointes, a reentrant rhythm with a constantly varying circuit.[6] 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),[10] as well as northeastern Thailand (idiopathic VF/Brugada syndrome).[11] 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[12] :

  • Hypertrophic cardiomyopathy
  • Right ventricular cardiomyopathy (ARVD)
  • 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,[13] and Timothy syndrome[14] ). 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 5 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 ECG during rest will likely be normal.

CPVT may be caused by mutations in the CASQ2 or RYR2 genes.[15] 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 4 genes that encode sarcomeric proteins— TNNT2, MYBPC3, MYH7, ­and TNNI3 —account for approximately 90% of cases.[16] Most people with hypertrophic cardiomyopathy who have symptoms 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 and arrhythmogenic 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. Eight genes (TGFB3, RYR2, DSP, PKP2, DSG2,[17] TMEM43, and JUP) and 4 additional loci (14q12-q22, 2q32.1-32.3, 10p14-p12, and 10q22) have been implicated in the pathogenesis of this disorder, which is inherited in an autosomal dominant fashion with incomplete penetrance. Those 8 genes are believed to be responsible for approximately 40-50% of the total cases of ARVD.[17]

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.[18]

Brugada syndrome can be caused by many genes. Currently, 8 genes are known to cause Brugada syndrome (SCN5A, GPD1L, CACNA1C, CACNB2, SCN1B, KCNE3, SCN3B, and HCN4), but they account for no more than 25% of cases. 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 1 case, however, these disorders were ruledout, and the patient was found to have a somatic mutation in the GNAI2 gene.[19]

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Epidemiology

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 VF, but 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.[20]

A prospective surveillance study gave a sudden death incidence of 53 per 100,000 population, accounting for 5.6% of all mortality.[21] 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 SVTs (PSVTs).[22] 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).[23] 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 ARVD (a 2-fold male predominance) and Brugada syndrome (an approximately 8-fold male predominance).

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Prognosis

The prognosis in patients with VT varies with the specific cardiac process but 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.

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.[24]

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.

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Contributor Information and Disclosures
Author

Steven J Compton, MD, FACC, FACP, FHRS Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP, FHRS is a member of the following medical societies: American College of Physicians, American Heart Association, American Medical Association, Heart Rhythm Society, Alaska State Medical Association, American College of Cardiology

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society

Disclosure: Nothing to disclose.

Acknowledgements

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Steven A Conrad, MD, PhD Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center

Steven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical Society, Shock Society, Society for Academic Emergency Medicine, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Ian S deSouza, MD Assistant Professor, Department of Emergency Medicine, Kings County Hospital/SUNY Downstate Medical Centers

Ian S deSouza, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Brian Olshansky, MD Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine

Brian Olshansky, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, and Heart Rhythm Society

Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting

Justin D Pearlman, MD, ME, PhD, FACC, MA Chief, Division of Cardiology, Director of Cardiology Consultative Service, Director of Cardiology Clinic Service, Director of Cardiology Non-Invasive Laboratory, Director of Cardiology Quality Program KMC, Dartmouth-Hitchcock Medical Center, Dartmouth Medical School

Justin D Pearlman, MD, ME, PhD, FACC, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America

Disclosure: Nothing to disclose.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Che' Damon Ward, MD Staff Physician, Department of Emergency Medicine, State University of New York Health Science Center at Brooklyn

Che' Damon Ward, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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ECG shows rapid monomorphic ventricular tachycardia (VT), 280 beats/min, associated with hemodynamic collapse. Tracing was obtained from patient with severe ischemic cardiomyopathy during electrophysiologic study. Single external shock subsequently converted VT to sinus rhythm. Patient had 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, ventricular rate is simply too fast for P waves to be observed. VT at 240-300 beats/min is often termed ventricular flutter.
ECG shows slow monomorphic ventricular tachycardia (VT), 121 beats/min, from patient with old inferior wall myocardial infarction and well-preserved left ventricular (LV) function (ejection fraction, 55%). Patient presented with symptoms of palpitation and neck fullness. Note ventriculoatrial dissociation, most obvious in V2 and V3. Slower VT rates and preserved LV function are associated with better long-term prognosis.
At first glance, tracing suggests rapid polymorphic ventricular tachycardia. This is actually sinus rhythm with premature atrial complex and superimposed lead motion artifact. Hidden sinus beats can be observed by using calipers to march backwards from final 2 QRS complexes. This artifact can be generated easily with rapid arm motion (eg, brushing teeth) during telemetry monitoring.
Torsades de pointes. Image A: This is polymorphic ventricular tachycardia associated with resting QT-interval prolongation. In this case, it was caused by class III antiarrhythmic agent sotalol. This rhythm is also observed in families with mutations affecting certain cardiac ion channels. Image B: Torsades de pointes, a form of ventricular tachycardia. Courtesy of Science Source/BSIP.
Preexcited atrial fibrillation. Patient has accessory atrioventricular connection. Atrial fibrillation has been induced. Conduction over accessory pathway results in wide QRS complex, mimicking ventricular tachycardia.
Curative ablation of ventricular tachycardia (VT). Patient had VT in setting of ischemic cardiomyopathy. VT was induced in electrophysiology laboratory, and ablation catheter was placed at critical zone of slow conduction within VT circuit. Radiofrequency (RF) energy was applied to tissue through catheter tip, and VT terminated when critical conducting tissue was destroyed.
Ventricular pacing at 120 beats/min. Newer pacemakers use bipolar pacing. If smaller pacing stimulus artifact is overlooked, erroneous diagnosis of ventricular tachycardia may result. Because leads are most commonly placed in right ventricular apex, paced beats will have left bundle-branch block morphology with inferior axis. Causes of rapid pacing include (1) tracking of atrial tachycardia in DDD mode, (2) rapid pacing due to rate response being activated, and (3) endless loop tachycardia. Application of magnet to pacemaker will disable sensing and allow further diagnosis.
Supraventricular tachycardia with aberrancy. Tracing is from patient with structurally normal heart who has normal resting ECG. This rhythm is orthodromic reciprocating tachycardia with rate-related left bundle-branch block. Note relatively narrow RS intervals in precordial leads.
Termination of ventricular tachycardia (VT) with overdrive pacing. Patient has reentrant VT, which is terminated automatically by pacing from implantable cardioverter-defibrillator.
Posteroanterior view of right ventricular endocardial activation map during ventricular tachycardia in patient with prior septal myocardial infarction. Earliest activation is recorded in red, late activation as blue to magenta. Fragmented low-amplitude diastolic local electrograms were recorded adjacent to earliest (red) breakout area, and local ablation in this scarred zone (red dots) resulted in termination and noninducibility of this previously incessant arrhythmia.
Monomorphic ventricular tachycardia.
Polymorphic ventricular tachycardia.
ECG from 32-year-old woman with recent-onset heart failure and syncope.
ECG from 48-year-old man with wide-complex tachycardia during treadmill stress test. Any wide-complex tachycardia tracing should raise possibility of ventricular tachycardia, but closer scrutiny confirms left bundle-branch block conduction of supraventricular rhythm. By Brugada criteria, RS complexes are apparent in precordium (V2-V4), and interval from R wave onset to deepest part of S wave is < 100 ms in each of these leads. Ventriculoatrial dissociation is not seen. Vereckei criteria are based solely upon aVR, which shows no R wave, initial q wave width < 40 ms, and no initial notching in q wave. Last Vereckei criterion examines slope of initial 40 ms of QRS versus terminal 40 ms of QRS complex in aVR. In this case, initial downward deflection in aVR is steeper than terminal upward deflection, yielding Vi/Vt ratio >1. All of these criteria are consistent with aberrantly conducted supraventricular tachycardia. Gradual rate changes during this patient's treadmill study (not shown here) were consistent with sinus tachycardia mechanism.
ECG shows form of idiopathic ventricular tachycardia (VT) seen in absence of structural heart disease. This rhythm arises from 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 wide QRS complex and conducted atrial beat, confirming atrioventricular dissociation and VT mechanism.
Wide QRS complex tachycardia is evident on ECG from 64-year-old man with history of prior myocardial infarction (MI) and syncope. In patients with prior MI, most common mechanism of wide QRS complex tachycardia is ventricular tachycardia.
Atrioventricular dissociation.
Fusion beats, capture beats, and atrioventricular dissociation.
Retrograde P waves.
Retrograde P waves.
Torsades de pointes.
H and E, intermediate power of a healed myocardial infarct. Areas of fibrosis (pale pink) dissect between myocytes (red).
 
 
 
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