Wide complex tachycardias

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Wide complex tachycardia is a cardiac rhythm of more than 100 beats per minute with a QRS duration of 120 milliseconds or more. It is critical to differentiate whether the wide complex tachycardia is of ventricular origin and is ventricular tachycardia (VT), or if it is of supraventricular origin with aberrant conduction (SVT with aberrancy). Rapid differentiation between these two causes of wide complex tachycardia is absolutely critical because the treatment options are quite different for VT versus SVT with aberrancy. Wide complex tachycardia should be assumed to be due to ventricular tachycardia even in a hemodynamically stable patient unless proven otherwise, and first line treatment with verapamil should be avoided.

A wide complex tachycardia is either of ventricular origin (ventricular tachycardia or VT), of supraventricular origin with aberrant conduction (SVT with aberrancy), of supraventricular origin and is conducted down a bypass tract such as in Wolff-Parkinson-White syndrome (WPW), or is due to a pacemaker malfunction. Approximately 80% of wide complex tachycardias are due to ventricular tachycardia.^[1]

For more detailed information regarding how to differentiate VT from SVT please view the differential diagnosis page or click here.

Differentiating between VT and SVT as the cause of wide complex tachycardia is absolutely critical because the treatment options are quite different for VT versus SVT with aberrancy.

The diagnosis of VT is more likely if:

• There is a history of myocardial infarction, myocardial ischemia, heart failure 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
• The morphology of the QRS complexes resembles that of a previous premature ventricular contraction (PVC).
• 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]

The diagnosis of atrial fibrillation with aberrant conduction should be considered if

• The heart rate is over 200 beats per minute
• If the rhythm is grossly irregularly irregular

The diagnosis of rapid conduction down a bypass tract due to ventricular pre-excitation such as Wolff-Parkinson-White syndrome (WPW) should be considered if

• There is intermittent present of a Delta wave
• There is intermittently a short PR interval

A paced rhythm as a cause of wide complex tachycardia is infrequent. This diagnosis is suggested if

• A pacemaker is in place and there is a LBBB pattern with superior left axis deviation, however, depending on the site of pacing this pattern can vary significantly
• A wide complex tachycardia can be due to an SVT if the pacemaker is tracking sensed atrial activity and is pacing the ventricles rapidly as result
• Pacemaker-mediated tachycardia may be present if there is retrograde conduction which triggers atrial activity during ventricular pacing.
• Runaway pacemaker syndrome in which the pacemaker fires at a rate of nearly 2000 bpm and captures intermittently
• Sensor induced tachycardia in which case the pacemaker fires at a rate of nearly 160-180 bpm in response to electrocautery, noise, vibration, limb movement or other stimuli.

• ECG artifact
• Ventricular fibrillation is usually more chaotic

The underlying cause of wide complex tachycardia tends to be ventricular tachycardia (VT) in patients > 35 years of age (sensitivity of 92% and a positive predictive value of 85% for VT) and supraventricular tachycardia (SVT) with aberrancy in patients < 35 years of age (positive predictive value of approximately 70%).^[3]

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.^[3] 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).

Wide complex tachycardia is defined as a heart rate > 100 beats per minute and a QRS duration > 120 ms.

VT with right bundle branch block morphology: AV dissociation is present, the QRS interval is greater than 140 ms, and the complexes are all up right in the anterior precordial leads consistent with ventricular tachycardia as the origin of the rhythm.

---

Shown below is a patient with sinus tachycardia and WPW which mimics VT: A Delta wave consistent with pre-excitation is present.

Electroyte abnormalities such as hypokalemia (which can be associated with ventricular tachycardia), and hypomagnesemia (which can lead to Torsade de Pointes) should be ruled out.

The management of wide complex tachycardia should begin by assessing the patient’s ABCs (airway, breathing, and circulation). If the patient is unstable and either hypotension, altered mental status, chest pain, heart failure or seizures are present, then immediate synchronized cardioversion should be performed. If the patient is stable, the optimal management depends upon the differentiation of ventricular tachycardia versus supraventricular tachycardia with aberrant conduction as a cause of the wide complex tachycardia. Treatment targeted at the underlying cause can then be initiated. A wide complex tachycardia should be assumed to be and managed as though it is due to ventricular tachycardia until proven otherwise. This is true even in a hemodynamically stable patient until proven otherwise (VT can often be hemodynamically stable). The initial management strategy includes avoiding the use of a long acting AV nodal blocking agent and drugs that suppress left ventricular contractility such as verapamil which can induce hypotension in a previously stable patient.

Wide complex tachycardia QRS ≥ 120ms

Do the following simultaneously: – Assess and support ABC’s as needed – Give oxygen – Monitor ECG, BP, oxymetry – Identify and treat reversible causes (hypokalemia, hypomagnesemia

Is the patient stable? Unstable signs include: – Chest pain – Congestive heart failure – Hypotension – Loss of consciousness – Seizures

Yes

No

Is the rhythm regular?

Immediate synchronized cardioversion -Establish IV access – Give IV sedation if the patient is conscious – Consider expert consultation

Regular rhythm

Irregular rhythm

Ventricular tachycardia or uncertain rhythm?

Confirmed SVT with aberrancy?

Afib with aberrancy?

Pre-excited Afib (Afib + WPW)?

Recurrent polymorphic VT?

Torsade de pointes?

– Give amiodarone 150 mg IV over 10 min – Repeat amiodarone as needed for a maximal dose of 2.2g/24h – Prepare for elective synchronized cardioversion

– If certain VT is not present, give adenosine 6 mg rapid IV push – If no conversion give 12 mg IV push – May repeat 12 mg dose once

– Consider expert consultation – Control rate e.g diltiazem or beta blockers Use beta blockers with caution in pulmonary diseases or CHF

– Consider expert consultation – Avoid AV nodal blocking agents e.g adenosine, digoxin, diltiazem and verapamil – Consider amiodarone 150 mg IV over 10 min

Consider expert consultation

Load with Magnesium 1-2 g over 5-60 min, then infusion

Algorithm based on the 2003 ACLS guidelines for the management of tachycardia.^[4]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

A wide complex tachycardia (WCT) is either of ventricular origin (ventricular tachycardia), of supraventricular origin with aberrant conduction (SVT with aberrancy), of supraventricular origin and is conducted down a bypass tract such as in Wolff-Parkinson-White syndrome (WPW), or is due to a pacemaker malfunction. The most common cause of WCT is ventricular tachycardia (VT), which accounts for 80% of all cases of WCT.^[1][2] Supraventricular tachycardia (SVT) with aberrancy accounts for 15% to 20% of WCTs. SVTs with preexcitation and antidromic atrioventricular reentrant tachycardia account for 1% to 6% of WCTs.^[3]

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

• STEMI
• Unstable angina

• AV reentrant tachycardia
• Pre-excitation syndrome
• Supraventricular tachycardia
• Ventricular tachycardia

Cardiovascular	Acute coronary syndrome, Andersen cardiodysrhythmic periodic paralysis, arrhythmogenic right ventricular dysplasia, AV block, cardiomyopathy, catecholaminergic polymorphic ventricular tachycardia, congenital heart disease, congestive heart failure, hypertrophic cardiomyopathy, ischaemic heart disease, Jervell and Lange-Nielsen syndrome, long QT Syndrome, myocardial Infarction, myocarditis, NSTEMI, 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	Arsenic trioxide, arsenicals
Dermatologic	No underlying causes
Drug Side Effect	Alimemazine, almokalant, amiodarone, amitriptyline, amphetamines, antiarrhythmics, asenapine, astemizole, azimilide, azithromycin, bepridil, bretylium, budipine, chloroquine, cibenzoline, cisapride, citalopram, clomipramine, clozapine, cocaine, crizotinib, desipramine, digitalis, diphenhydramine, disopyramide, dofetilide, dolasetron, doxepin, dronedarone, droperidol, eribulin mesylate, fluconazole, grepafloxacin, halofantrine, haloperidol, ibutilide, imipramine, indapamide, inotropes, ketanserin, ketoconazole, lidoflazine, lubeluzole, methadone, methadyl acetate, methamphetamine, midodrine, mizolastine, moxifloxacin, naratriptan, nicardipine, nilotinib, ondansetron, pasireotide, pazopanib, pentamidine, phenothiazines, pimozide, piperaquine, prenylamine, probucol, procainamide, propoxyphene, quinidine, quinine, ranolazine, retigabine, ritodrine, ritonavir, saquinavir, sertindole, sotalol, sparfloxacin, sympathomimetic agents, tedisamil, telithromycin, terfenadine, terodiline, tetrabenazine, thioridazine, vandetanib, vemurafenib, venlafaxine, vernakalant, voriconazole, vorinostat, ziprasidone, zotepine, zuclopenthixol
Ear Nose Throat	No underlying causes
Endocrine	Hyperthyroidism, hypothyroidism, pheochromocytoma
Environmental	Hypothermia, zero gravity
Gastroenterologic	No underlying causes
Genetic	Channelopathies, myotonic dystrophy, Andersen cardiodysrhythmic periodic paralysis, Jervell and Lange-Nielsen syndrome, 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, electrophysiologic studies, heart surgery, pulmonary artery catheter , right heart catheterisation
Infectious Disease	No underlying causes
Musculoskeletal / Ortho	Andersen cardiodysrhythmic periodic paralysis, Timothy syndrome, myotonic dystrophy
Neurologic	No underlying causes
Nutritional / Metabolic	Acidosis, acid-base disturbances, 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, asenapine, astemizole, azimilide, azithromycin, bepridil, bretylium, budipine, chloroquine, cibenzoline, cisapride, citalopram, clomipramine, clozapine, cocaine, crizotinib, desipramine, digitalis, diphenhydramine, disopyramide, dofetilide, dolasetron, doxepin, dronedarone, droperidol, eribulin mesylate, fluconazole, grepafloxacin, halofantrine, haloperidol, ibutilide, imipramine, indapamide, inotropes, ketanserin, ketoconazole, lidoflazine, lubeluzole, methadone, methadyl acetate, methamphetamine, midodrine, mizolastine, moxifloxacin, naratriptan, nicardipine, nilotinib, ondansetron, pasireotide, pazopanib, pentamidine, phenothiazines, pimozide, piperaquine, prenylamine, probucol, procainamide, propoxyphene, quinidine, quinine, ranolazine, retigabine, ritodrine, ritonavir, saquinavir, sertindole, sotalol, sparfloxacin, sympathomimetic agents, tedisamil, telithromycin, terfenadine, terodiline, tetrabenazine, thioridazine, vandetanib, vemurafenib, venlafaxine, vernakalant, voriconazole, vorinostat, ziprasidone, zotepine, zuclopenthixol
Psychiatric	Anorexia nervosa, starvation
Pulmonary	Hypoxia, obstructive sleep apnea, sleep apnea
Renal / Electrolyte	Acidosis, acid-base disturbances, acute starvation, electrolyte imbalance, hyperkalaemia, hypocalcemia, hypoglycaemia, hypokalemia, hypomagnesemia
Rheum / Immune / Allergy	No underlying causes
Sexual	No underlying causes
Trauma	Myocardial contusion
Urologic	No underlying causes
Dental	No underlying causes
Miscellaneous	No underlying causes

• Congestive heart failure
• Hypokalemia
• Hypomagnesemia
• STEMI

• Arrhythmogenic right ventricular dysplasia
• Hypertrophic cardiomyopathy
• Long QT syndrome
• Myocarditis
• 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

• Supraventricular tachycardia (SVT) with aberrant ventricular conduction is either new or due to a preexisting left or right bundle branch block or a preexisting nonspecific intraventricular conduction delay (IVCD). The underlying supraventricular rhythm that is aberrantly conducted can be any one of the following rhythms:

• Atrial flutter with 2:1 conduction and occasional 1:1 conduction
• Automatic junctional tachycardia
• AV nodal reentrant tachycardia
• AV reentrant tachycardia using a bypass tract
• Intraatrial reentrant tachycardia
• Paroxysmal atrial tachycardia
• SA nodal reentrant tachycardia
• Sinus tachycardia

The diagnosis of rapid antegrade conduction down a bypass tract due to ventricular pre-excitation such as Wolff-Parkinson-White syndrome (WPW) should be considered if

• There is intermittent present of a delta wave
• There is intermittently a short PR interval

A paced rhythm as a cause of wide complex tachycardia is infrequent. This diagnosis is suggested in the following scenarios:

• A pacemaker is in place and there is a LBBB pattern with superior left axis deviation, however, depending on the site of pacing this pattern can vary significantly
• A wide complex tachycardia is due to an SVT and the pacemaker is tracking sensed atrial activity and is pacing the ventricles rapidly as result
• Pacemaker-mediated tachycardia in which there is retrograde conduction which triggers atrial activity during ventricular pacing
• Runaway pacemaker syndrome in which the pacemaker fires at a rate of nearly 2000 bpm and captures intermittently
• Sensor induced tachycardia in which case the pacemaker fires at a rate of nearly 160-180 bpm in response to electrocautery, noise, vibration, limb movement or other stimuli

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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 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 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. These three historical features have positive predictive values for VT of > 95% in a small study, but sensitivities of 66%, 24%, and 24%, respectively.^[1] 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).^[2]

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. ^[3]

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 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%^[4]

• The lead II R-wave-peak-time: sensitivity 60%, specificity 82.7%^[5]

• The aVR algorithm: sensitivity 87.1%, specificity 48%^[6]

• The Bayesian algorithm: sensitivity 89%, specificity 52%^[7]

• The Griffith algorithm: sensitivity 94.2%, specificity 39.8%^[8]

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.^[5] 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.^[10]

• 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.^[6]

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.^[12]

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.^[13]

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.^[14][15] Verapamil should be avoided in patients with wide complex tachycardia as it can result in hemodynamic deterioration in patients with ventricular tachycardia.^[16]

Arrhythmia	Rhythm	Rate	P wave	PR Interval	QRS Complex	Response to Maneuvers	Epidemiology	Co-existing Conditions
Atrial Fibrillation (AFib)[17][18]	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[19]	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)[20][21][22][23]	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[24][25]	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)[26][27]	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[28][29]	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)[30][31][32]	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[33][34]	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

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

The underlying cause of wide complex tachycardia tends to be ventricular tachycardia (VT) in patients > 35 years of age (sensitivity of 92% and a positive predictive value of 85% for VT) and supraventricular tachycardia (SVT) with aberrancy in patients < 35 years of age (positive predictive value of approximately 70%).^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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.^[1] 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).

• Antiarrhythmics
• Amphetamines
• Cocaine
• Droperidol
• Inotropes
• Phenothiazines
• Sympathomimetic agents

• Arrhythmogenic right ventricular dysplasia
• Channelopathies
• Hemochromatosis
• Long QT syndrome
• Rheumatoid arthritis
• Sarcoidosis
• Short QT syndrome
• Systemic lupus erythematosus
• Tetralogy of Fallot

• Alcohol
• Anemia
• Anxiety
• Caffeine
• Chocolate
• Fever
• Hyperthyroidism
• Hypokalemia
• Hypomagnesemia
• Hypoxia
• Myocardial ischemia
• Menstruation
• Psychological stress
• Pulmonary embolism
• Stimulants
• Tea
• Theobromine
• Theophylline

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