Ventricular tachycardia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-in Chief: Avirup Guha, M.B.B.S.[2]

In 1906 Gallavardin discovered the reasons behind the cardiac instability which leads to ventricular tachycardia, and put forth the idea that VT could convert into ventricular fibrillation. Thomas Lewis gave the first electrocardiographic description of ventricular tachycardia in 1909. It was first suggested in 1921 that coronary occlusion could the main cause of ventricular tachycardia. Many advancements have been made in the diagnosis and management protocols of ventricular tachycardia (VT) since that time.

• The first electrocardiographic description and evidence of ventricular tachycardia (VT) was given by Thomas Lewis in 1909.^[1]
  • He described a patient with shortness of breath, precordial pain, and dropsy in whom he observed from three to eleven successive extrasystoles.
  • He deduced from the electrocardiogram, venous pulse recording, and clinical evidence that the rhythm was of ventricular origin.

• In 1906, Einthoven had recorded ventricular premature beats and ventricular bigeminy using his string galvanometer.^[2]

• In 1906 Gallavardin did landmark work in France in which he found the reasons for instability in VT and its ability to convert in ventricular fibrillation.^[3][4]
  • He challenged the fact that ventricular tachycardia was no more than a succession of extrasystoles suggesting that although the two phenomena were intimately related, the same mechanism might not be responsible for both.

• Lewis and Smith did experimentation with dogs by simulating VT by ligating coronary arteries and were able to find characteristics of VT as we have described in the other sections.^[5][6]

• Robinson and Herrmann, in 1921, suggested that coronary occlusion was a frequent cause of ventricular tachycardia and the prognosis in these cases appeared to be poor.^[7]
• They also suggested the most initial criteria for VT classification.

• That was modified later by Rosenberg as well as Dressler and Roesler who pointed out the occasional occurrence of fusion beats in tracings showing the arrhythmia.^[8][9]

• Since then we have come a long way in making of the diagnostic criteria better with advent of esophageal and venous leads and invasive electrophysiologic studies.^[10][11][12]

• Holter and colleagues devised radio signal technique for obtaining a longer period of observation of the patient’s rhythm.^[13]
• Later in development portable battery-operated electromagnetic tape recording with high-speed analyzing equipment was described by Holter and has been called Holter monitor ever since.^[13]
• This technique has led to discovery, classification and research for treatment of various forms of VT.

• Direct intracavitary recordings from the human ventricle were reported by Lenegre and Maurice in 1945.
• Hiss bundle electrocardiograms were described by Ciraud, Latour, and Puech in 1960.^[14][15]

• It was only in 1969, however, that a safe, percutaneous method of recording the His bundle electrocardiogram in man was reported.^[16]
• Intracardiac recordings have allowed more precise diagnosis of ventricular tachycardia and have modified the electrocardiographic criteria for diagnosing this arrhythmia.^[10]

• In 1972, Wellens et al. reported the initiation and termination of ventricular tachycardia in patients with priorventricular tachycardia using critically timed extrastimuli.^[17]
• This ability to initiate and terminate arrhythmias under controlled circumstances, as well as the ability to record from multiple sites within the heart, has allowed rapid advancement in our understanding of cardiac arrhythmias.

• Initially phlebography was very popular amongst scientists for features of VT.
• Prinzmetal and Kellogg in 1934 concluded that slower, independent A waves might be encountered in two-thirds of cases of VT.^[18]

• Schrire and Vogelpoel discovered that the so-called cannon A is encountered in presence of atrioventricular dissociation, but could occur in regular fashion at the same rate in nodal tachycardias.^[19]

• The AV dissociation and its reflection was demonstrated by Wilson et al. in 1964. ^[20]

• Levine was the first who noted slight irregularity in cycle length in patients with ventricular tachycardia which was audible with the stethoscope.^[21] In 1927, he mentioned variation in intensity of the first heart sound, due to atrioventricular dissociation, and extended these observations in conjunction with Harvey in 1948.^[22][23]

• Harvey and Corrado demonstrated multiple low-frequency sounds audible in ventricular tachycardia as a differential point.^[24]

• In 1930, Strauss^[25] correlated prognosis with the presence or absence of organic heart disease. It was noted that 60% of the cases occurred during the fifth and sixth decade of life, with a male preponderance.

• Congestive heart failure was present in two-thirds of the patient population and digitalis had been administered before the onset of the tachycardia in half of the patients.
• Quinidine sulfate was acutely successful in controlling paroxysms in all cases in which it was employed. There were many other case series which had similar findings.^{[26][27][28][29][30][31][32][33]}

• Most investigators classified ventricular tachycardia into two forms on the basis of pattern and duration of the arrhythmia.
• Intermittent ventricular tachycardia was defined as runs of ventricular tachycardia separated by periods of normal rhythm, the latter often showing ventricular extrasystoles or short paroxysms of tachycardia lasting seconds or minutes which ceased spontaneously or were controlled readily in most cases by therapy. Persistent ventricular tachycardia was thereby defined as being of longer duration and without periods of interruption.^[34]

• Several authors found important differences in prognosis between these groups.^[34][33][35]

• In all these series, the prognosis in patients with no identified organic heart disease was better than in those patients with abnormal hearts.
• Paroxysmal ventricular tachycardia in young patients with otherwise apparently healthy hearts was thought by several investigators to run a benign clinical course.^[30][36]

• With the advent of more refined investigations such as cardiac catheterization, echocardiography, and endomyocardial biopsy, anatomic and histologic details were found about the primary electrical disease.

• Various investigators attempted to ascribe prognostic significance to morphologic characteristics of ventricular tachycardia. Lundy and McLellan categorized ventricular tachycardia by bundle branch pattern and assumed incorrectly the ventricular origin of the tachycardia from these morphologies.^[26]

• A distinctive form of ventricular tachycardia with beat-to-beat alteration of QRS axis in a single lead has been called bidirectional tachycardia and was first described by Schwensen in 1922.^[37]
  • He observed its occurrence during atrial fibrillation and linked it to digitalis intoxication.

• Palmer and White reported its poor prognosis.^[38]
• The studies which followed showed the same finding of poor prognosis with digitalis.^[39][33]

• Scott in 1922 described a patient in whom quinidine could both terminate and prevent episodes of ventricular tachycardia.^[40]
  • He also noticed that on discontinuing quinidine ventricular tachycardia recurred. He also hypothesized that quinidine abolished ventricular tachycardia by lengthening the refractory period of the ventricle, thereby preventing early premature ventricular beats.

• Drury and others demonstrated that quinidine prolonged the refractory period of ventricular muscle in dogs.^[41]

• Levine and Fulton noted that treatment with quinidine could either terminate episodes of ventricular tachycardia or it could cause them.^[42]

• By 1950, Armbrust and Levine had followed a large population of patients and strongly advocated quinidine administration in the acute setting despite the difficulties associated with its use.^[32]

• Procainamide was used to treat ventricular tachycardia in man in 1950 and rapidly achieved widespread use.^[43][44]

• The first steps toward the development of procainamide had taken place many years earlier.
• In 1937, Beck and Mantz demonstrated that the topical application of procaine to the epicardium during surgical procedures reduced the occurrence of ventricular extrasystoles.^[45]

• Procaine was limited to use under anesthesia because of its central nervous system toxicity.
• With further development of newer congeners, procainamide and lidocaine achieved wide clinical use.

• Lidocaine was synthesized in 1946 and was first used clinically by Southworth and colleagues to prevent ventricular arrhythmias during cardiac catheterization.^[46]

• Other antiarrhythmic drugs quickly followed procainamide and lidocaine. Phenytoin was first used to treat ventricular tachycardia in 1958.^[47]

• In the 1960s a number of other drugs including beta-adrenergic blocking agents, disopyramide, bretylium, mexiletine and amiodarone were reported to be effective in treating ventricular arrhythmias in selected patients.^[48]

• Once ventricular tachycardia had accelerated and become less organized, the likelihood of successful termination of the arrhythmia by drugs became more remote. Considerable experimental work had demonstrated the feasibility of using electric shocks to terminate ventricular fibrillation in a variety of experimental situations.^[49][50]

• Several chance events and experimental procedure had demonstrated the use of this procedure.^[51][52]

• In 1961, Alexander et al. used alternating current electively for the first time to terminate ventricular tachycardia that could not be stopped by giving antiarrhythmic drugs.^[53]

• Over the subsequent few years, Lown and his colleagues greatly refined and popularized techniques for terminating tachyarrhythmias by electric discharges.^{[54][55][56][57]}

• Direct current (DC) or capacitor discharge was shown to be safer and more effective than alternating current.
• Synchronization of the direct current discharge to the R-wave resulted in safer termination of arrhythmias and was called cardioversion and was used for different kinds of arrhythmias.

• Ventricular tachycardia could occasionally be terminated by thumping the chest in some patients.^[58]

• Defibrillation even using DC discharge required much higher energies, however. These techniques were quickly accepted around the world and truly revolutionized the treatment of cardiac tachyarrhythmias.
• Implantable devices capable of sensing and terminating ventricular tachycardia automatically by either defibrillation or cardioversion have come into clinical use.^[59]

• In 1960, Zoll and associates reported that increasing the heart rate by closed-chest cardiac stimulation had prevented recurrent ventricular tachyarrhythmias.^[60]
• They demonstrated that runs of ventricular fibrillation could be prevented by pacing the heart above a certain critical heart rate.

• In the same year, Schwedel, Escber. and Furman demonstrated similar short-term benefit from transvenous right ventricular endocardial pacing. ^[61]

• Both the above experiments were in patients with heart block. Subsequently, Sowton and colleagues applied a similar technique in patients with ventricular tachycardia and fibrillation but without evidence of heart block.^[62]

• Apparently, pacing prevented episodes of tachyarrhythmia and extrasystoles in these patients. Furthermore, these authors suggested that the combined use of antiarrhythmic drugs and overdrive pacing might be better than the use of either modality alone in some patients.

• There were many case series and reports of the use of overdrive pacing after this.
• These series are small with a limited follow-up period. Not all reports were favorable and long-term outcomes were rarely available.
• Acute treatment of ventricular arrhythmias by overdrive pacing became accepted as effective in some patients.

• In 1959 Couch reported on a patient in whom ventricular aneurysmectomy was successfully performed to prevent recurrent ventricular tachycardia.^[63][64]
• But the procedure has been associated with poor success rates and surgical mortality of 20-50%.^[65][66]

• Newer techniques include incising the margins of an aneurysm and excising these, and extensive endocardial scar excision combined with aneurysmectomy.^{[67][68][69][70]}

• Sympathectomy, myocardial revascularization, and mitral valve replacement have also been tried for VT repair.^[71]

Year	Event
1909	First electrocardiographic demonstration of ventricular tachycardia.
1921	Relationship of coronary artery disease and ventricular tachycardia described.
1921	Electrocardiographic criteria for ventricular tachycardia were defined.
1922	Quinidine used to treat ventricular tachycardia.
1946	Lidocaine synthesized.
1950	Procainamide introduced into clinical practice.
1956	Alternating current used to terminate ventricular tachycardia.
1959	Aneurysmectomy performed to treat ventricular tachycardia.
1960	Use of cardiac pacing to prevent ventricular tachycardia in patients with complete heart block.
1960	Elective alternating current termination of ventricular tachycardia.
1962	Synchronized cardioversion of ventricular tachycardia.
1966	Torsades de pointes described.
1971	Ventricular tachycardia initiated and terminated by critically-timed premature ventricular beats.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Sara Zand, M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]

Ventricular tachycardia refers to a rhythm with a heart rate in excess of 100 (and in some definitions 120) beats per minute that arises distal to the bundle of His. Ventricular tachycardia can be classified based on morphology and duration of tachyarrhythmia. The morphology of the QRS complexes on the ECG maybe (monomorphic ventricular tachycardiaor polymorphic ventricular tachycardia). In sustained VT duration of VT lasts > 30 sec or VT< 30 sec that needs to termination due to compromised hemodynamic. Nonsustained, or unsustained VT is more than 3 consecutive premature ventricular complexes with spontaneously termination. Bidirectional VT is a type of VT with beat to beat changing QRS frontal plane axis indicating of digoxin toxicity or catecholaminergic polymorphic VT.Torsades de pointed is a type of polymorphic VT in the setting of long QT interval which is characterized by twisting of the points, waxing and waning QRS amplitude, Long-short sequence with long-coupling interval to the first VT beat, maybe initiated after bradycardia such as high grade AV block.Ventricular flutter is explained as a regular ventricular arrhythmia with rate about 300 beat per minute (bpm), or cycle length 200 ms, sinusoidal monophorphic QRS complexes, Without any isoelecterical interval between successive QRS complexes. Ventricular fibrillation is a rapid, grossly irregular electrical activity with variation in morphologic waveforms by ventricular rate >300bpm, cycle length <200 ms. VT/ VF storm is an electerical storm or cardiac instability due to ≥ 3 episodes of sustained VT, VF or shock delivery from ICD within 24 hours.

Term	Definition	Feature
Ventricular tachycardia[1]	Presence of ≥ 3 consecutive premature ventricular complexes with the rate of >100 beats per minute or cycle length< 600 ms	[2]
	Sustained VT	VT> 30 sec VT< 30 sec that needs to termination due to compromised hemodynamic
	Nonsustained, or unsustained VT	≥3 consecutive premature ventricular complexes, spontaneously termination
	Monomorphic VT	Uniform and stable beat to beat QRS morphology
	Polymorphic VT	Changing beat to beat QRS morphology
	Bidirectional VT	VT with beat to beat changing QRS frontal plane axis, indicator of digoxin toxicity or catecholaminergic polymorphic VT
Torsades de pointes	A type of polymorphic VT Occurance in the setting of long QT interval Characterised by twisting of the points, waxing and waning QRS amplitude Long-short sequence with long-coupling interval to the first VT beat Maybe initiated after bradycardia such as high grade AV block	[3]
Ventricular flutter	A regular ventricular arrhythmia Rate about 300 beat per minute (bpm), or cycle length 200 ms Sinusoidal monophorphic QRS complexes Without any isoelecterical interval between successive QRS complexes	[4]
Ventricular fibrillation	Rapid, grossly irregular electrical activity Variation in morphologic waveforms Ventricular rate >300bpm, cycle length <200 ms	[5]
VT, VF storm	Electerical storm or cardiac instability due to ≥ 3 episodes of sustained VT, VF or shock delivery from ICD within 24 hours

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Avirup Guha, M.B.B.S.[2]; Mugilan Poongkunran M.B.B.S [3]

Ischemic heart disease is a common cause of ventricular tachycardia. Other causes of ventricular tachycardia include congenital heart disease, valvular heart disease, dilated non-ischemic cardiomyopathy, sarcoidosis, infiltrative cardiomyopathy, inflammatory cardiomyopathy, and inherited channelopathies. In addition, illicit drug use with sympathetic activity such as cocaine and methamphetamine, and drugs with QT interval prolongation effect and also electrolyte disturbances such as hypokalemia, hypomagnesemia, and hypocalcemia may cause ventricular tachycardia.

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. They are mainly due to acute conditions that promote rapid dysfunction of automaticity and include:^[1][2][3][4]

• Acute coronary syndrome
• Congestive heart failure
• NSTEMI
• STEMI
• Unstable angina

• Acid-base disturbances
• Antiarrhythmics
• Azithromycin
• Cardioversion
• Clarithromycin
• Claritin
• Cocaine
• Congestive heart failure
• Dilated cardiomyopathy
• Erythromycin
• Hypokalemia
• Hypomagnesemia
• Myocarditis
• Obstructive sleep apnea
• Pulmonary artery catheter
• STEMI
• Tricyclic antidepressants

Cardiovascular	Acute coronary syndrome, Andersen cardiodysrhythmic periodic paralysis, arrhythmogenic right ventricular dysplasia, AV block, Brugada syndrome, cardiomyopathy, catecholaminergic polymorphic ventricular tachycardia, congenital heart disease, congestive heart failure, dilated cardiomyopathy, hypertensive heart disease, hypertrophic cardiomyopathy, ischemic heart disease, Jervell and Lange-Nielsen syndrome, long QT syndrome, mitral valve prolapse, myocardial infarction, myocarditis, noncompaction cardiomyopathy, NSTEMI, QT lengthening, right ventricular outflow tract tachycardia, Romano-Ward syndrome, short QT syndrome, short QT syndrome type 1, short QT syndrome type 2, short QT syndrome type 3, short QT syndrome type 4, short QT syndrome type 5, STEMI, Timothy syndrome, torsade de pointes, unstable angina, valvular heart disease, ventricular aneurysm, Wolff-Parkinson-White syndrome
Chemical / poisoning	Acetaminophen, arsenic trioxide, arsenicals, methanol, aconitine
Dermatologic	No underlying causes
Drug Side Effect	Acetaminophen, alimemazine, almokalant, amiodarone, amitriptyline, amphetamines, antiarrhythmics, asenapine, aspirin, astemizole, azimilide, azithromycin, bepridil, bretylium, bromocriptine, budipine, chloroquine, cibenzoline, cisapride, citalopram, claritin, clomipramine, clozapine, cocaine, crizotinib, desipramine, digitalis, diphenhydramine, disopyramide, dofetilide, dolasetron, doxepin, dronedarone, droperidol, Eletriptan, eribulin mesylate, erythromycin, fluconazole, fosphenytoin, grepafloxacin, halofantrine, haloperidol, ibutilide, imipramine, indapamide, inotropes, ketanserin, ketoconazole, lidoflazine, lubeluzole, methadone, methadyl acetate, methamphetamine, midodrine, mizolastine, moxifloxacin, naratriptan, nicardipine, nilotinib, Nizatidine, ondansetron, pasireotide, pazopanib, pentamidine, pergolide, phenothiazines, pimozide, piperaquine, prenylamine, probucol, procainamide, propoxyphene, quinidine, quinine, ranolazine, retigabine, ritodrine, ritonavir, saquinavir, sertindole, sotalol, sparfloxacin, sumatriptan, sympathomimetic agents, tedisamil, telithromycin, terfenadine, terodiline, tetrabenazine, theophylline, thioridazine, tricyclic antidepressants, vandetanib, vemurafenib, venlafaxine, vernakalant, voriconazole, vorinostat, ziprasidone, zotepine, zuclopenthixol
Ear Nose Throat	No underlying causes
Endocrine	Addisonian crisis, Cushing’s syndrome, diabetic ketoacidosis, hyperthyroidism, hypothyroidism, myxedema, pheochromocytoma
Environmental	Heat stroke, hypothermia, zero gravity
Gastroenterologic	No underlying causes
Genetic	Andersen cardiodysrhythmic periodic paralysis, channelopathies, Fabry disease, Jervell and Lange-Nielsen syndrome, myotonic dystrophy, Romano-Ward syndrome, short QT syndrome type 1, short QT syndrome type 2, short QT syndrome type 3, short QT syndrome type 4, short QT syndrome type 5, Timothy syndrome
Hematologic	No underlying causes
Iatrogenic	Cardioversion, defibrillation, heart surgery, post-anesthesia, pulmonary artery catheter, right heart catheterisation, runaway pacemaker syndrome, cardiac transplantation
Infectious Disease	Chagas heart disease, Lyme disease, myocarditis
Musculoskeletal / Ortho	Andersen cardiodysrhythmic periodic paralysis, Timothy syndrome, myotonic dystrophy
Neurologic	Acute stroke
Nutritional / Metabolic	Acid-base disturbances, acidosis, acute starvation, electrolyte imbalance, hyperkalaemia, hypocalcemia, hypoglycaemia, hypokalemia, hypomagnesemia
Obstetric/Gynecologic	No underlying causes
Oncologic	No underlying causes
Opthalmologic	No underlying causes
Overdose / Toxicity	Alimemazine, almokalant, amiodarone, amitriptyline, amphetamines, antiarrhythmics, bretylium, budipine, chloroquine, cibenzoline, cisapride, clomipramine, clozapine, crizotinib, desipramine, digitalis, diphenhydramine, disopyramide, dofetilide, doxepin, dronedarone, droperidol, eribulin mesylate, halofantrine, haloperidol, ibutilide, lidoflazine, methadone, methadyl acetate, methamphetamine, midodrine, mizolastine, pentamidine, phenothiazines, pimozide, piperaquine, prenylamine, probucol, procainamide, propoxyphene, quinidine, quinine, ranolazine, retigabine, ritodrine, ritonavir, sertindole, tedisamil, telithromycin, terfenadine, terodiline, tetrabenazine, thioridazine, vandetanib, vemurafenib, venlafaxine, voriconazole, ziprasidone, zotepine, zuclopenthixol
Psychiatric	Anorexia nervosa, major depression, Takotsubo cardiomyopathy
Pulmonary	Chronic pulmonary artery hypertension, COPD, hypoxia, obstructive sleep apnea
Renal / Electrolyte	Acid-base disturbances, acidosis, electrolyte imbalance, hyperkalaemia, hypocalcemia, hypoglycaemia, hypokalemia, hypomagnesemia, renal failure, uremia
Rheum / Immune / Allergy	Amyloidosis, cardiac sarcoidosis, giant cell myocarditis, rheumatoid arthritis, systemic lupus erythematosus
Sexual	No underlying causes
Trauma	Blunt chest trauma, myocardial contusion
Urologic	No underlying causes
Dental	No underlying causes
Miscellaneous	Alcoholism, idiopathic

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [2] Syed Hassan A. Kazmi BSc, MD [3]

When wide QRS tachycardia is present on the [[electrocardiogram] ECG, it is necessary to rapidly differentiate whether it is caused by ventricular tachycardia (VT) or a supraventricular tachycardia (SVT) with aberrant conduction. While the ECG provides the most reliable data to distinguish VT from SVT with aberrant conduction, the clinical history and the age of the patient may also provide additional discriminatory information regarding the cause of the wide QRS tachycardia. While older patients with a prior history of myocardial infarction are more likely to have VT, young hemodynamically stable patients presenting with paroxysmal tachycardia are more likely to have SVT with aberrant conduction. Nevertheless, the primary tool to differentiate VT from SVT with aberrant conduction is the ECG. There are several findings that are more common in ventricular tachycardia, and there are also more sophisticated electrophysiologic algorithms such as the Brugada and Vereckei algorithms that can be used to distinguish VT from SVT with aberrant conduction. The diagnosis of VT is more likely if: There is a history of myocardial infarction or structural heart disease, the electrical axis is -90 to -180 degrees (a “northwest” or “superior” axis), the QRS is > 140 msec, there is AV dissociation, there are positive or negative QRS complexes in all the precordial leads, and the morphology of the QRS complexes resembles that of a previous premature ventricular contraction (PVC).

• Risk factors for the ventricular tachycardia as a cause of wide complex tachycardia include a history of prior myocardial infarction, a history of congestive heart failure, and a history of recent angina pectoris.^[1]
• Wide complex tachycardia will be due to VT in 98% of cases if there’s a history of structural heart disease.

• Hemodynamic stability does not reliably differentiate VT from SVT.
• Patients with ventricular tachycardia can often be hemodynamically stable, and stable vital signs do not rule out ventricular tachycardia.
• This is often a major mistake on the part of clinicians and can lead to inappropriate treatment of VT as SVT with poor outcomes. ^[2]

Although AV dissociation is highly suggestive of VT, it may also be seen in junctional tachycardias with retrograde block.

Example: Shown below is a wide complex tachycardia. AV dissociation is present as shown by the varying morphology highlighted by the red arrows. LBBB configuration. The absence of RS in the chest leads. The diagnosis is VT.

Example: Shown below is a wide complex tachycardia. AV dissociation is present as shown by the varying morphology highlighted by the red arrows. LBBB configuration. The absence of RS in the chest leads. The diagnosis is VT.

• A wide complex tachycardia with a RBBB morphology and a QRS > 0.14, or a LBBB morphology with a QRS > 0.16 suggests VT.

• The finding of a positive or negative QRS complex in all precordial leads is in favor of ventricular tachycardia.
• A monophasic or biphasic RBBB QRS complex in V1. But none of their patients with SVT had a preexisting RBBB. Therefore, this finding is of limited importance (A Wellens criterion).
• 80 to 85% of aberrant beats have a RBBB pattern, but ectopic beats that arise from the LV have a similar morphology.
• LBBB with a rightward axis
• LBBB with the following QRS morphology:

• R wave in V1 or V2 > 0.03 second
• Any Q wave in V6
• Onset of the QRS to nadir of the S wave in V1 > 0.06 seconds
• Notching of the S wave in V1 or V2

Morphological criteria
LBBB pattern
Initial R more than 40 ms?	Yes ≥ VT
Slurred or notched downwards leg of S wave in leads V1 or V2?	Yes ≥ VT
Beginning of Q to nadir QS > 60 ms in V1 or V2?	Yes ≥ VT	LR > 50:1
Q or QS in V6?	Yes ≥ VT	LR > 50:1
RBBB pattern
Monophasic R or qR in V1?	Yes ≥ VT
R taller than R’ (rabbit-ear sign)?	Yes ≥ VT	LR > 50:1
rS in V6?	Yes ≥ VT	LR > 50:1

• If premature ventricular contractions (PVCs) are present on a prior tracing, and if the morphology of the wide complex tachycardia is the same, then it is likely to be ventricular tachycardia.
• Previous EKG may show a preexisting intraventricular conduction delay (IVCD) which would favor SVT with abberancy.
• If there are premature atrial contractions (PAC)s with aberrant conduction, then the origin of the wide complex tachycardia may be supraventricular.

Example: Shown below is a wide complex tachycardia. There is no AV dissociation. A RBBB morphology is present. The wide complex tachycardia resembles sinus rhythm from the same patient. The diagnosis in this patient is SVT with RBBB:

Shown below is the ECG from the same patient as above in sinus rhythm. The QRS complex is very similiar to that during the wide complex tachycardia:

• A “northwest axis” with a QRS axis in the RUQ between -90 and +180 degrees favors ventricular tachycardia.

The image below illustrates the “Northwest axis”also known as “Extreme Right Axis” or “No Man’s Land”:

• Rare, but one of the strongest pieces of evidence in favor of VT.
• SVT with aberrancy rarely follows a beat with a short cycle length.

Fusion beats are rare, but strongly suggests VT.

• VT is generally not affected by vagal stimulation.
• May terminate reentrant arrhythmias

• A pacing wire is placed in the RA and the atrium is stimulated at a rate faster than the tachycardia.
• If ventricular capture occurs and the QRS is normal in duration, then one can exclude the possibility of aberrant conduction.

• Diagnosis of SVT made if the episode is initiated by a premature P wave.
• If the paroxysm begins with a QRS then the tachycardia may be either ventricular or junctional in origin.
• If the first QRS of the tachycardia is preceded by a sinus p wave with a PR interval shorter than that of the conducted sinus beats, the tachycardia is ventricular.

• In SVT, each QRS is preceded by a His bundle potential.
• In VT there is no preceding His deflection.
• The retrograde His deflection is usually obscured by the much larger QRS complex.

• VT (slight irregularity of RR)
• SVT with aberrancy: Sinus, atrial tachycardia (AT), or flutter
• Antidromic atrioventricular reentrant tachycardia (AVRT)

• The first 50 beats of VT can be irregular
• SVT with aberrancy: Atrial fibrillation, multifocal atrial tachycardia (MAT)
• Atrial fibrillation with bypass tract usch as WPW is a dangerous cause of a very rapid irregular rhythm as the atrial rate is conducted rapidly over the bypass tract. Shown below is the tracing of a patient with atrial fibrillation conducting down the bypass tract in WPW. Note that the rate is extremely rapid, and the rhythm is irregularly irregular. It is critical that this rhythm be recognized to avoid the administration of agents that would further accelerate conduction down the accessory pathway in this patient with WPW which could cause degeneration into ventricular fibrillation. The best treatment for this patient is Pronestyl 15 mg/kg load over 30 minutes then 2-6 mg/min gtt or DC cardioversion:

• The mechanism of SVT with aberrancy is usually concealed retrograde conduction. The ventricular beat penetrates the right branch (RB) or left branch (LB). When the next supraventricular activation front occurs that bundle is refractory and if conduction can occur, it will proceed down the other bundle. Since the RB has a longer refractory period than the LB, a right bundle branch block (RBBB) morphology is more common.
• Other mechanisms of “rate related aberrancy” are preexisting bundle branch block (BBB), physiologic (phase 3) aberration and use dependent aberration secondary to medication. In physiologic aberration, the stimulus comes to the His-Purkinje system before it has fully recovered from the previous stimulus. The ensuing activation is either blocked or conducts slowly. Again, the RB is the one more at risk. Most commonly seen at the onset of paroxysmal supraventricular tachycardia (PSVT), but can become sustained.
• In use-dependent aberration, a patient on and anti-arrhythmic (especially class Ic agents) will have a progressive decrement in ventricular conduction rate the more it is stimulated. During faster heart rates, less time is available for the drug to dissociate from the receptor and an increased number of receptors are blocked.

Several ECG criteria and algorithms have been used to differentiate VT and SVT, the common one of which is Brugada algorithm. Below is a list of all algorithms:

• Brugada algorithm: sensitivity 89%, specificity 59.2%^[3]

• The lead II R-wave-peak-time: sensitivity 60%, specificity 82.7%^[4]

• The aVR algorithm: sensitivity 87.1%, specificity 48%^[5]

• The Bayesian algorithm: sensitivity 89%, specificity 52%^[6]

• The Griffith algorithm: sensitivity 94.2%, specificity 39.8%^[7]

In 2010 Joseph Brugada et al. published a new criterion to differentiate VT from SVT in wide complex tachycardias: the R wave peak time (RWPT) in Lead II.^[4] To aplly the criteria, the duration of onset of the QRS to the first change in polarity (either nadir Q or peak R) is measured in lead II as shown below. If the RWPT is ≥ 50ms the likelihood of a VT very high (positive likelihood ratio 34.8). This criterion was successful in their own population of 163 selected patients and is awaiting prospective testing in a larger trial.

Example: As shown below, an R-wave to Peak Time (RWPT) of ≥ 50ms in lead II strongly suggests VT:

Absence of an RS complex in all precordial leads?

Yes? VT (SN=0.21 SP=1.0)

No?

R to S interval>100 ms in one precordial lead?

Yes? VT (SN=0.66 SP=0.98)

No?

AV dissociation?

Yes? VT (SN=0.82 SP=0.98)

No?

Morphology criteria for VT present both in precordial leads V1, V2 and V6?

Yes? VT (SN=0.987 SP=0.965)

No?

SVT (SN=0.965 SP=0.987)

Based on the 2011 Nature Reviews Cardiology algorithm of broad complex tachycardia.^[9]

• An algorithm has been proposed by Vereckei and colleagues, wherein in addition to do the traditional criteria, the voltage change on the EKG is used as a final discriminatory criteria.
• In this method, the voltage change during the initial 40 ms (V_i) and the terminal 40 ms (V_t) of the same QRS complex is used to estimate the (V_i) and terminal (V_t) ventricular activation velocity ratio (V_i/V_t).
• A V_i/V_t > 1 suggests SVT and a V_i/V_t ≤ 1 suggests VT.^[5]

AV dissociation present?

Yes? VT

No?

Initial R wave in aVR present?

Yes? VT

No?

QRS morphology unlike BBB or FB?

Yes? VT

No?

Vi/Vt≤1?

Yes? VT

No?

SVT

Based on the 2011 Nature Reviews Cardiology algorithm of broad complex tachycardia.^[11]

Shown below is an image demonstrating the method used to calculate Vi/Vt. In this tracing, Vi/Vt is < 1 is suggestive of ventricular tachycardia according to Vereckei criteria.

Pacer spikes are present. There is a ventricular-paced rhythm at or near the upper rate limit at approximately 120-130 beats per minute. Given the mechanical nature of the trigger, the EKG is absolutely regular.

Shown below is a rhythm strip demonstrating pacemaker mediated tachycardia:

Wide QRS complex tachycardia (QRS duration greater than 120 ms)

Regular or irregular?

Regular

Irregular

Is QRS identical to that during SR? If yes, consider: – SVT and BBB – Antidromic AVRT

Atrial fibrillation Atrial flutter / AT with variable conduction and: a) BBB or b) Antegrade conduction via AP

Vagal maneuvers or adenosine

Previous myocardial infarction or structural heart disease? If yes, VT is likely.

1 to 1 AV relationship?

Yes or unknown

No

V rate faster than A rate

A rate faster than V rate

QRS morphology in precordial leads

VT

Atrial tachycardia Atrial flutter

Typical RBBB or LBBB

Precordial leads: – Concordant – No R/S pattern – Onset of R to nadir longer than 100ms

RBBB pattern: – qR, Rs or Rr’ in V1 – Frontal plane axis range from +90 degrees to -90 degrees

LBBB pattern: – R in V1 longer than 30 ms – R to nadir of S in V1 greater than 60 ms – qR or qS in V6

SVT

VT

VT

VT

The above algorithm is adapted from the 2003 American College of Cardiology.^[12]

Although termination of a wide complex tachycardia by either adenosine, a calcium channel blocker, a beta blocker or digoxin is suggestive of supraventricular tachycardia with aberrant conduction, VT can also be terminated by these pharmacotherapies.^[13][14] Verapamil should be avoided in patients with wide complex tachycardia as it can result in hemodynamic deterioration in patients with ventricular tachycardia.^[15]

Arrhythmia	Rhythm	Rate	P wave	PR Interval	QRS Complex	Response to Maneuvers	Epidemiology	Co-existing Conditions
Atrial Fibrillation (AFib)[16][17]	Irregularly irregular	On a 10-second 12-lead EKG strip, multiply number of QRS complexes by 6	Absent Fibrillatory waves	Absent	Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction	Does not break with adenosine or vagal maneuvers	2.7–6.1 million people in the United States have AFib 2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib	Elderly Following bypass surgery Mitral valve disease Hyperthyroidism Diabetes Heart failure Ischemic heart disease Chronic kidney disease Heavy alcohol use Left chamber enlargement
Atrial Flutter[18]	Regular or Irregular	75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) beats per minute (bpm), but 150 is more common	Sawtooth pattern of P waves at 250 to 350 bpm Biphasic deflection in V1	Varies depending upon the magnitude of the block, but is short	Less than 0.12 seconds, consistent, and normal in morphology	Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm	Incidence: 88 per 100,000 individuals	Elderly Alcohol
Atrioventricular nodal reentry tachycardia (AVNRT)[19][20][21][22]	Regular	140-280 bpm	Slow-Fast AVNRT: Pseudo-S wave in leads II, III, and AVF Pseudo-R’ in lead V1. Fast-Slow AVNRT P waves between the QRS and T waves (QRS-P-T complexes) Slow-Slow AVNRT Late P waves after a QRS Often appears as atrial tachycardia. Inverted, superimposed on or buried within the QRS complex (pseudo R prime in V1/pseudo S wave in inferior leads)	Absent (P wave can appear after the QRS complex and before the T wave, and in atypical AVNRT, the P wave can appear just before the QRS complex)	Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction QRS alternans may be present	May break with adenosine or vagal maneuvers	60%-70% of all supraventricular tachycardias	Structural heart disease Atrial tachyarrhythmias
Multifocal Atrial Tachycardia[23][24]	Irregular	Atrial rate is > 100 beats per minute	Varying morphology from at least three different foci Absence of one dominant atrial pacemaker, can be mistaken for atrial fibrillation if the P waves are of low amplitude	Variable PR intervals, RR intervals, and PP intervals	Less than 0.12 seconds, consistent, and normal in morphology	Does not terminate with adenosine or vagal maneuvers	0.05% to 0.32% of electrocardiograms in general hospital admissions	Elderly Chronic obstructive pulmonary disease (COPD)
Paroxysmal Supraventricular Tachycardia	Regular	150 and 240 bpm	Absent Hidden in QRS	Absent	Narrow complexes (< 0.12 s)	Breaks with vagal maneuvers, adenosine, diving reflex, oculocardiac reflex	Prevalence: 0.023 per 100,000	Alcohol Caffeine Nicotine Psychological stress Wolff-Parkinson-White syndrome
Premature Atrial Contractrions (PAC)[25][26]	Regular except when disturbed by premature beat(s)	80-120 bpm	Upright	> 0.12 second May be shorter than that in normal sinus rhythm (NSR) if the origin of PAC is located closer to the AV node Ashman’s Phenomenon: PAC displaying a right bundle branch block pattern	Usually narrow (< 0.12 s)	Breaks with vagal maneuvers, adenosine, diving reflex, oculocardiac reflex		Infants Cardiomyopathy Myocarditis Elderly Coronary artery disease Stroke Increased atrial natriuretic peptide (ANP) Hypercholesterolemia
Wolff-Parkinson-White Syndrome[27][28]	Regular	Atrial rate is nearly 300 bpm and ventricular rate is at 150 bpm	With orthodromic conduction due to a bypass tract, the P wave generally follows the QRS complex, whereas in AVNRT, the P wave is generally buried in the QRS complex.	Less than 0.12 seconds	A delta wave and evidence of ventricular pre-excitation if there is conduction to the ventricle via ante-grade conduction down an accessory pathway A delta wave and pre-excitation may not be present because bypass tracts do not conduct ante-grade.	May break in response to procainamide, adenosine, vagal maneuvers	Worldwide prevalence of WPW syndrome is 100 – 300 per 100,000	Ebstein’s anomaly Mitral valve prolapse: This cardiac disorder, if present, is associated with left-sided accessory pathways. Hypertrophic cardiomyopathy: This disorder is associated with familial/inherited form of WPW syndrome. Hypokalemic periodic paralysis Pompe disease Tuberous sclerosis
Ventricular Fibrillation (VF)[29][30][31]	Irregular	150 to 500 bpm	Absent	Absent	Absent (R on T phenomenon in the setting of ischemia)	Does not break in response to procainamide, adenosine, vagal maneuvers	3-12% cases of acute myocardial infarction (AMI) Out of 356,500 out of hospital cardiac arrests, 23% have VF as initial rhythm	Myocardial ischemia / infarction Cardiomyopathy Channelopathies e.g. Long QT (acquired / congenital) Electrolyte abnormalities (hypokalemia/hyperkalemia, hypomagnesemia) Aortic stenosis Aortic dissection Myocarditis Cardiac tamponade Blunt trauma (Commotio Cordis) Sepsis Hypothermia Pneumothorax Seizures Stroke
Ventricular Tachycardia[32][33]	Regular	> 100 bpm (150-200 bpm common)	Absent	Absent Initial R wave in V1, initial r > 40 ms in V1/V2, notched S in V1, initial R in aVR, lead II R wave peak time ≥50 ms, no RS in V1-V6, and atrioventricular dissociation	Wide complex, QRS duration > 120 milliseconds	Does not break in response to procainamide, adenosine, vagal maneuvers	5-10% of patients presenting with AMI	Coronary artery disease Aortic stenosis Cardiomyopathy Electrolyte imbalances (e.g., hypokalemia, hypomagnesemia) Inherited channelopathies (e.g., long-QT syndrome) Catecholaminergic polymorphic ventricular tachycardia Arrhythmogenic right ventricular dysplasia Myocardial infarction Torsades de pointes is a form of polymorphic VT that is often associated with a prolonged QT interval

The table below provides information on the differential diagnosis of ventricular tachycardia in terms of ECG appearance:

Disease Name	Causes	ECG Characteristics	ECG view
Ventricular tachycardia [34][35][36][37][38]	Ischemic heart disease Illicit drug use such as cocaine and methamphetamine Structural heart diseases Electrolyte disturbances Congestive heart failure Myocarditis Obstructive sleep apnea Pulmonary artery catheter Long QT syndrome	Ventricular tachycardia originates from a ventricular focus. Lasts more than 30 seconds. Broad QRS complexes: rate of >90 BPM.	[39]
Ventricular fibrillation [32][40][41][42]	Acute coronary ischemia Cardiomyopathies Congenital heart disease Myocardial infarction Heart surgery Electrolyte abnormalities	Poorly identifiable QRS complexes and absent P waves The heart rate is >300 BPM Rhythm is irregular	[43]
Ventricular flutter [44][45][46]	Electrolyte disturbances Medications such as: Disopyramide Quinidine	The ECG shows: A typical sinusoidal pattern Frequency of 300 bpm	[47]
Asystole [48][49]	Hypovolemia Hypoxia Acidosis Hypothermia Hyperkalemia or Hypokalemia Hypoglycemia Cardiac Tamponade Tension pneumothorax Thrombosis Myocardial infarction Thrombosis Pulmonary embolism Cardiogenic shock Degeneration of the sinoatrial or atrioventricular nodes Ischemic stroke	There is no electrical activity in the asystole	[50]
Pulseless electrical activity [51][52]	Hypovolemia Hypoxia Hydrogen ions (Acidosis) Hypothermia Electrolyte disturbances Hypoglycemia Tablets or Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants, or calcium channel blockers Tamponade Tension pneumothorax Thrombosis (Myocardial infarction) Thrombosis (Pulmonary embolism) Trauma (Hypovolemia from blood loss)	Several pattern are possible including: Normal sinus rhythm Sinus tachycardia, with discernible P waves and QRS complexes Bradycardia, with or without P waves	[53]
Torsade de Pointes [54][55][56]	*Electrolyte disturbances Medications such as: Amiodarone Azithromycin Clozapine Famotidine Flecainide Foscarnet Levofloxacin Lithium Mirtazipine Quetiapine Risperidone Tacrolimus Tamoxifen Ziprasidone	Paroxysms of VT with irregular RR intervals. A ventricular rate between 200 and 250 beats per minute. Two or more cycles of QRS complexes with alternating polarity. Changing amplitude of the QRS complexes in each cycle in a sinusoidal fashion. Prolongation of the QT interval. Is often initiated by a PVC with a long coupling interval, R on T phenomenon. There are usually 5 to 20 complexes in each cycle.	[57]

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