Pulseless ventricular tachycardia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2]

Pulseless ventricular tachycardia is an often fatal cardiac dysrhythmia where the regular rhythmic contraction of the heart is replaced by non-rhythmic, faster, yet inadequate contractions. 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, pulselessness and sudden death. In 1909,Thomas Lewis gave the first electrocardiographic description of ventricular tachycardia. It was also first implied in 1921 that coronary occlusion could be the main incriminating factor of any ventricular tachycardia. The ineffective contractions in pulseless ventricular tachycardia do not appropriately perfuse the organ, leading to ischemia as well as heart failure. This condition requires immediate medical attention as it is an emergency and can lead to ventricular fibrillation and sudden death. As a result of markedly rapid ventricular contractions, diastole is shortened and there is a significant decrease in the ventricular filling. This results in a significant reduction in cardiac output, and an absent pulse. Pulseless ventricular tachycardia refers to a rhythm with a heart rate above 120 beats per minute, wide QRS complexes above 120 milliseconds, the dissociation between the atria and ventricles, presence of fusion beats, and an electrical axis between -90 to -180. Because the majority of wide complex tachycardia cases will be ventricular tachycardia, any wide complex tachycardia should always be assumed to be due to ventricular tachycardia until proven otherwise.

There is limited information about the historical perspective of Pulseless ventricular tachycardia.

Pulseless ventricular tachycardia as a ventricular tachycardia may be classified based on the morphology of the QRS complexes into two subtypes/groups: monomorphic ventricular tachycardia, and polymorphic ventricular tachycardia.

Rapid abnormal automaticity and triggered activity are thought to be the main electrophysiological mechanisms of pulseless ventricular tachycardia.

Structural heart disease is the most common cause of pulseless ventricular tachycardia. Other causes include but are not limited to, drugs/medications, congenital heart diseases, not to mention congenital and inherited channelopathies. It is important to note that QT interval lengthening medications, as well as electrolyte disturbances, can also result in pulseless ventricular tachycardia.

Pulseless ventricular tachycardia must be differentiated from other diseases that cause wide complex tachycardia, such as supraventricular tachycardia with aberrant conduction, SVT with pre-excitation and antidromic atrioventricular reentrant tachycardia

Ventricular tachycardia and ventricular fibrillation are the causes of most sudden cardiac deaths and account for about 300,000 deaths per year in the united states alone. This figure is most likely underestimated as it doesn’t account for deaths due to unwitnessed dysrhythmias. The majority of deaths due to ventricular arrhythmias occur In adults over 35 years of age.

Risk factors for pulseless ventricular tachycardia as a cause of wide complex tachycardia includes any disease or condition that stresses or damages myocardial tissue. A family history of ventricular tachycardia or other rhythm disturbances may increase risk, while some lifestyle changes or medications may decrease risk.

According to the 2017 American Heart Association guidelines screening of first-degree relatives is recommended when a patient presents with any of the symptoms or has a positive family history of conditions like QT syndrome, hypertrophic, dilated cardiomyopathy and right ventricular dysplasia.

On initial presentation, patients with impending pulseless ventricular tachycardia may show signs of inadequate cardiac perfusion such as chest pain, shortness of breath, diaphoresis, palpitations, and syncope. Physical examination may be positive for hypotension, tachycardia, tachypnea, increased JVD, and an S1. Eventually, Pulseless ventricular tachycardia ensues and patients become unconscious and unresponsive with no detectable pulse. If defibrillation is not begun as soon as possible patients may progress to cardiac arrest and death.

The diagnosis of pulseless ventricular tachycardia is based on ECG and physical examination findings. An ECG should be the initial study, and other investigations may be carried out afterward to determine the underlying etiology.

Pulseless ventricular tachycardia may be symptomatic or asymptomatic. In a young patient with a family history of sudden death, immediate evaluation for an inherited ventricular syndrome is recommended. If symptomatic, the ventricular rate, duration of tachycardia, and the presence of underlying disease determine the kind of symptoms that present.

Physical examination should consist of a thorough cardiac exam, lung exam, and close monitoring of vital signs. Physical examination may be positive for hypotension, tachycardia, tachypnea, increased JVD, and an S1.

There aren’t any specific findings associated with pulseless ventricular tachycardia. However, investigations such as serial cardiac enzymes, serum electrolytes, and toxicology screen should be conducted to find the underlying etiology of the arrhythmia.

An ECG is very helpful in the diagnosis of Pulseless ventricular tachycardia. Findings on an ECG suggestive or diagnostic of Pulseless ventricular tachycardia include regular R-R intervals, rapid ventricular rate with an indistinguishable atrial rate (absence of p-waves), Av dissociation, and a wide QRS complex (more 0.12 sec).

There are no x-ray findings associated with Pulseless ventricular tachycardia.

There are no specific echocardiography/ultrasound findings associated with pulseless ventricular tachycardia. However, echocardiography/ultrasound may be helpful in the evaluation of underlying etiologies in patients as well as complications due to the arrhythmia.

There are no specific MRI findings associated with pulseless ventricular tachycardia. However, a cardiac MRI may be helpful when structural heart disease is implicated as an etiology and the assessment provided by echocardiography is not satisfactory. A cardiac MRI is particularly helpful in the evaluation of structural heart disease i.e arrhythmogenic right ventricular cardiomyopathy as well it’s infiltrative diseases such as sarcoidosis.

2017 guidelines from the AHA/ACC/HRS state that MRI, cardiac computed tomography (CT), or radionuclide angiography can be useful in detecting and characterizing underlying heart disease when echocardiography fails to provide an accurate evaluation of LV or RV function and/or assessment of structural changes. Electrophysiologic (EP) testing can be useful when an uncertain diagnosis of sustained monomorphic ventricular tachycardia. An electrophysiological study is especially useful for assessing the risk of ventricular tachycardia in patients with ischemic cardiomyopathy, non-ischemic cardiomyopathy, or adult congenital heart disease who have syncope or other ventricular arrhythmia symptoms and who do not meet indications for a primary prevention implantable cardioverter-defibrillator.

Medical therapy with IV vasopressors and antiarrhythmic medications i.e amiodarone, is usually simultaneous with defibrillation. 1mg 1V of epinephrine administered every 3-5 minutes or, a single dose of 40 units IV of vasopressin can be used as vasopressors.

Immediate defibrillation is the main intervention for pulseless ventricular tachycardia.

Surgery is not a mainstay or a preferred method of treatment for pulseless ventricular tachycardia.

Implantable cardiac defibrillators are recommended in high-risk patients i.e, patients with dilated cardiomyopathy for the primary prevention of pulseless ventricular tachycardia.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2]

There is limited information about the historical perspective of Pulseless ventricular tachycardia.

• There is limited information about the historical perspective of Pulseless ventricular tachycardia.

• Gallavardin in 1906 was responsible for the discovery of the rationale behind cardiac instability leading to ventricular tachycardia. He further put forth the idea that ventricular tachycardia could convert to ventricular fibrillation and lead to cardiac arrest and death.

• The first electrographic description of ventricular tachycardia was given by Thomas Lewis in 1909.

• Coronary occlusion was suggested to be the main cause of ventricular tachycardia in 1921.

• Several advancements have since been made in the diagnosis and management protocols on Ventricular tachycardia.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2]

Pulseless ventricular tachycardia may as a ventricular tachycardia be classified based on the morphology of the QRS complexes into two subtypes/groups: monomorphic ventricular tachycardia, and polymorphic ventricular tachycardia

Based on the morphology of the QRS complexes, ventricular tachycardia can be grouped into two types:

• In monomorphic ventricular tachycardia the more common form, the rhythm originates from a single focus within the ventricles and the QRS complexs within each lead are identical. This form of ventricular tachycardia is most commonly seen in patients with underlying structural heart diseases.

• In polymorphic ventricular tachycardia, there are multiple ventricular foci with the resultant QRS complexes varying from beat-to-beat. Torsade de Pointes is the most common form of polymorphic ventricular tachycardia and appears as a cyclical progressive change in the cardiac axis. The most common cause of polymorphic ventricular tachycardia is myocardial ischemia.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2] Cafer Zorkun, M.D., Ph.D. [3]

Rapid abnormal automaticity and triggered activity are thought to be the main electrophysiological mechanisms of pulseless ventricular tachycardia. In abnormal automatically, the ventricular myocytes produce strong, voluntary, and recurrent depolarization and subsequent contractions at a rate that is higher than normal. This is due to a due to a decrease (ranging between -70mV and -30mV) in normal resting membrane potential. The higher the reduction in membrane potential, the faster and more rapid the already abnormal automaticity. Triggered activity is used to depict the indication of impulse in cardiac myocytes that is dependent on afterdepolarizations (an oscillation in membrane potential that occurs after repolarization). Two types of afterdepolarizations have been identified: Early afterdepolarizations(EAD) and Delayed afterdepolarizations (DAD). When either of these afterdepolarizations become high enough to reach the membrane threshold, they result in a spontaneous “triggered” action potential. Hence for a triggered activity to occur, at least one action potential must precede it.

In pulseless ventricular tachycardia, the combination of increased automatically and/or triggered activity leads to a rate of contraction that is too rapid to result in adequate ventricular filling during diastole. This results in deficient cardiac output, inadequate perfusion of organs, and hemodynamic collapse.

The normal physiology of Pulseless ventricular tachycardia/ventricular tachycardia can be understood as follows:

Pathophysiology of ventricular tachycardia can be better studied depending upon the subclass:^[1][2][3][4]

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

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

• During VT cardiac output is reduced as a consequence of decreased ventricular filling from the rapid heart rate and the lack of properly timed or coordinated atrial contraction.
• Ischemia and mitral insufficiency 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.
• 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.

• There are two reasons the morphology of the QRS does not vary in monomorphic ventricular tachycardia:
  • A single site that generates automaticity of a single point in either the left or right ventricle.
  • A reentry circuit within the ventricle.

• Polymorphic ventricular tachycardia, on the other hand, is most commonly caused by abnormalities of ventricular muscle repolarization.
• The predisposition to this problem usually manifests on the ECG as a prolongation of the QT interval. QT prolongation may be congenital or acquired.
• Congenital problems include long QT syndrome and catecholaminergic polymorphic ventricular tachycardia.
• Acquired problems are usually related to drug toxicity or electrolyte abnormalities, but can occur as a result of myocardial ischemia.
• Class III anti-arrhythmic drugs such as sotalol and amiodarone prolong the QT interval and may in some circumstances be pro-arrhythmic.
• Other relatively common drugs including some antibiotics and antihistamines may also be a danger, particularly in combination with one another.
• Problems with blood levels of potassium, magnesium and calcium may also contribute. High dose magnesium is often used as an antidote in cardiac arrest protocols.

Autosomal-dominant mutations in ryanodine receptor type 2 ( ryr2) have been complicated in a type of ventricular tachycardia known as catecholaminergic polymorphic ventricular tachycardia.^[5]

Conditions associated with [disease name] include:

• Ventricular Tachychardia
• Venticular Fibrillation
• Pulseless electrical activity

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2] Avirup Guha, M.B.B.S.[3]; Mugilan Poongkunran M.B.B.S [4]

Structural heart disease is the most common cause of pulseless ventricular tachycardia. Other causes include but are not limited to, drugs/medications, congenital heart diseases, not to mention congenital and inherited channelopathies. It is important to note that QT interval lengthening medications, as well as electrolyte disturbances, can also result in pulseless 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. but are not limited to;^[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

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2] Homa Najafi, M.D.[3]Rim Halaby, M.D. [4] Syed Hassan A. Kazmi BSc, MD [5]

Pulseless ventricular tachycardia must be differentiated from other diseases that cause wide complex tachycardia, such as supraventricular tachycardia with aberrant conduction, SVT with pre-excitation and antidromic atrioventricular reentrant tachycardia.^[1] While an EKG 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 complex 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. These three historical features have positive predictive values for VT of > 95% in a small study, but sensitivities of 66%, 24%, and 24%, respectively.^[2] Wide complex tachycardia will be due to VT in 98% of cases if there’s a history of structural heart disease. Only 7% of patients with SVT with aberrancy will have had a prior myocardial infarction (MI).^[3]

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. ^[4]

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. 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. 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 aberrancy.
• 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 similar 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 suggest 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 such 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 is 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, 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 an 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%^[5]

• The lead II R-wave-peak-time: sensitivity 60%, specificity 82.7%^[6]

• The aVR algorithm: sensitivity 87.1%, specificity 48%^[7]

• The Bayesian algorithm: sensitivity 89%, specificity 52%^[8]

• The Griffith algorithm: sensitivity 94.2%, specificity 39.8%^[9]

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.^[6] To apply 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.^[11]

• 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 criterion.
• 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.^[7]

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.^[13]

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.^[14]

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.^[15][16] Verapamil should be avoided in patients with wide complex tachycardia as it can result in hemodynamic deterioration in patients with ventricular tachycardia.^[17]

Arrhythmia	Rhythm	Rate	P wave	PR Interval	QRS Complex	Response to Maneuvers	Epidemiology	Co-existing Conditions
Atrial Fibrillation (AFib)[18][19]	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[20]	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)[21][22][23][24]	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[25][26]	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)[27][28]	Regular except when disturbed by premature beat(s)	80-120 bpm	Upright	> 0.12 second Maybe 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[29][30]	Regular	Atrial rate is nearly 300 bpm and the 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)[31][32][33]	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[34][35]	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 [36][37][38][39][40]	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.	[41]
Ventricular fibrillation [34][42][43][44]	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	[45]
Ventricular flutter [46][47][48]	Electrolyte disturbances Medications such as: Disopyramide Quinidine	The ECG shows: A typical sinusoidal pattern Frequency of 300 bpm	[49]
Asystole [50][51]	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	[52]
Pulseless electrical activity [53][54]	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	[55]
Torsade de Pointes [56][57][58]	*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 the 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.	[59]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2]

Ventricular tachycardia and ventricular fibrillation^[1] are the causes of most sudden cardiac deaths and account for about 300,000 deaths per year in the united states alone. This figure is most likely underestimated as it doesn’t account for deaths due to unwitnessed dysrhythmias.^[2]

For more see Epidemiology and Demographics of ventricular tachycardia.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2] Aditya Ganti M.B.B.S. [3]

According to the 2017 American Heart Association guidelines screening of first-degree relatives is recommended when a patient presents with any of the symptoms such as QT syndrome, hypertrophic or dilated cardiomyopathy and right ventricular dysplasia.

According to the 2017 American Heart Association /American College of Cardiology/Heart Rhythm Society guideline screening of first-degree relatives is recommended when a patient is identified as having any of the following:^[1][2]

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

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aisha Adigun, B.Sc., M.D.[2]

On initial presentation, patients with impending pulseless ventricular tachycardia may show signs of inadequate cardiac perfusion such as chest pain, shortness of breath, diaphoresis, palpitations, and syncope. Physical examination may be positive for hypotension, tachycardia, tachypnea, increased JVD, and an S1. Eventually, Pulseless ventricular tachycardia ensues and patients become unconscious and unresponsive with no detectable pulse. If defibrillation is not begun as soon as possible patients may progress to cardiac arrest and death. ^[1]

• On initial presentation, patients with impending pulseless ventricular tachycardia may present with signs of inadequate cardiac perfusion such as chest pain, shortness of breath, diaphoresis, palpitations, and syncope.
• Physical examination may be positive for hypotension, tachycardia, tachypnea, increased JVD, and an S1.
• Eventually, Pulseless ventricular tachycardia ensues and patients become unconscious and unresponsive with no detectable pulse.^[1]

• Common complications of pulseless ventricular tachycardia include^[2][3]:
  • Cardiac arrest/sudden cardiac death
  • Anoxic brain injury and lifelong neurological complications
  • Post-cardiac arrest syndrome
  • Ischemic-reperfusion injury
  • Cardiomyopathy
  • Infection related to implantable cardioverter-defibrillator

• Prognosis of pulseless ventricular tachycardia is majorly based on two considerations; the presence of prior expressed or unexpressed cardiac issues, and the time from the beginning of the dysrhythmia to defibrillation and conversion to sinus rhythm and adequate perfusion.^[1]
• Up to 50% of patients who are defibrillated within seconds of the onset of tachycardia have high survival rates, while patients who experience delays of up to 15 minutes have a survival rate of as low as 5%.^[4]
• While the most significant factors affecting prognosis are underlying structural and ischemic cardiac issues, the presence of other comorbidities also play a significant role.^[1]

Template:WH Template:WS