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Wide QRS Complex Tachycardia

Authors

Manuel A. Obando1; Erin M. Marra2.

Affiliations
1 Aventura Hospital and Medical Center
2 Aventura Hospital and Medical Center

Last Update: June 26, 2023.

Continuing Education Activity

Wide complex tachycardia is a dysrhythmia with a long list of potential causes that ranges from various arrhythmias,
structural heart abnormalities, electrolyte disturbances, toxins, and many more. It is important to always assess a
patient’s hemodynamic status since there is a potential risk they could deteriorate rapidly. This activity reviews the
evaluation and management of wide complex tachycardia and explains the role of the interprofessional team in
improving the care for patients with this condition.

Objectives:

Describe the physical exam findings associated with wide complex tachycardia.

Explain the management of patients with wide complex tachycardia.

Outline the management of wide complex tachycardia.

Access free multiple choice questions on this topic.

Introduction
The heart has a complex electrical conduction system. This system is interwoven in the myocardium, which allows
the heart to beat at its own rhythm and creates what’s called a pulse (one of six important vital signs). The heart has
what is called a pacemaker, and its function is to determine how fast the heart will beat. It is because of this intricate
electrical system that allows all cardiac cells to beat (i.e., depolarize) in unison. A heartbeat (i.e., pulse) can be
classified as either regular versus irregular, fast versus slow, etc. When a person’s pulse falls out of what is considered
“normal,” then we say this individual has an arrhythmia. Electrocardiograms (a.k.a. EKGs or ECGs) are used to help
evaluate aberrancies in a patient’s heart rhythm and pulse. Arrhythmias can be classified by either how fast the heart is
beating, i.e., rate (tachycardia, bradycardia), the regularity of the heartbeat (regular, irregularly regular, or irregularly
irregular), and finally by the width of the QRS complex (narrow, wide). This article will be discussing a specific
group of arrhythmias – Wide QRS complex tachycardia (WTC).

It is important to go over some basic definitions describing what WCTs are, what causes them, how to diagnose them,
and how to manage/treat them. Tachycardia refers to a heart rate that is >100 beats per minute. The QRS complex
represents ventricular depolarization on the EKG. To briefly explain some cardiac anatomy, a normal heartbeat is
generated by an electrical stimulus that originates in the sino-atrial (SA) node. This stimulus then travels from the SA
node to the atrioventricular (AV) node. The normal conduction pathway for this electrical stimulus (which represents
the QRS) is from the AV node down the bundle of His, Purkinje fibers, and then into the ventricular myocardium
which causes them to contract (depolarize). The pathway just described is considered anterograde and orthodromic
because it follows the normal conduction circuit. When there are structural changes of the heart that can create
alternative conduction pathways, this can cause the electrical stimulus to go in reverse and would then be called
retrograde and antidromic. Depending on which pathway the electrical stimulus takes, it will affect how the QRS
complex will be visualized on the EKG. A normal QRS should be less than 0.12 seconds (120 milliseconds), therefore
a wide QRS will be greater than or equal to 0.12 seconds. To put it all together, a WCT is considered a cardiac
dysrhythmia that is > 100 beats per minute, wide QRS (> 0.12 seconds), and can have either a regular or irregular
rhythm.

This article will be covering WCT’s etiologies, epidemiology, evaluation, management, treatment, prognosis,
complications, and prevention. Of note, in an emergency situation where the patient is not clinically stable, it is
important for physicians to understand that correctly interpreting the type of WCT in this setting should not be their
primary concern. Rapidly and accurately diagnosing WCT still remains a problem because there are numerous
algorithms and complicated criteria that can be difficult to remember in an emergency setting. The most important
thing to do in such a situation is to stabilize the patient and just diagnose the WCT secondary to unknown origin or
etiology.[1][2][3]

Etiology
If a patient is clinically stable and time permits, knowing the cause of wide QRS complex tachycardia provides an
opportunity to appropriately manage the patient and significantly reduce the potential for morbidity and mortality.
Below are some of the known causes of WCT, which also consists of the differential diagnosis.[1][2]

Sodium channel blockade

Hyperkalemia

Hyper- or hypo-magnesemia

Supraventricular tachycardia (SVT) with pre-existing or a rate-related bundle branch block (BBB)

SVT with aberrant conduction

Atrial fibrillation (Afib) with Wolff-Parkinson-White syndrome (WPWS)

Mono-morphic ventricular tachycardia (VT)

Ventricular fibrillation (VFib)

Polymorphic VT (torsades de pointes)

Pacemaker mediated tachycardia (PMT)

Drug overdose and toxicities (i.e., TCA’s, digitalis, cocaine, lithium, diphenhydramine)

Post-resuscitation (ROSC)

EKG artifact

Epidemiology
Out of all the known causes for wide QRS complex tachycardia, there are two etiologies (VT, VF) that account for the
most cardiac deaths in the U.S. It is estimated that there are 300,000 deaths per year due to these cardiac
dysrhythmias. Between these two ventricular etiologies, VT tends to be the most common cause, accounting for
approximately 80% of WCTs. This is especially true in patients with a history of cardiovascular disease (i.e.,
myocardial infarctions, coronary artery disease) and increases the likelihood to 90%. SVT is the third most likely
cause of WCT, although it occurs less frequently. Out of the different causes of SVT, conduction with aberrancy
appears to be the most likely cause of WCT. SVT with aberrancy accounts for approximately 21% of WCTs.[3][4][5]

History and Physical

When first assessing these patients, the physician must act quickly and determine whether the patient is stable or
unstable. It is critical to first evaluate the patient’s ABCs (airway, breathing, circulation), which will guide your
management. Patients who are unstable due to WCT present with a myriad of symptoms such as altered mental status,
hypotension, pulmonary edema, or other signs of low end-organ perfusion (i.e., pallor, cyanosis, decreased body
temperature). Once a patient is deemed stable, a focused history and physical exam should be made quickly as a
patient’s clinical status can deteriorate suddenly. During an episode of WCT, patients will typically present with
persistent chest pain that may be accompanied by one or more of the following symptoms, such as shortness of breath,
diaphoresis, dizziness, and nausea.

A patient’s medical history provides significant information that can help the physician to determine the potential
cause of a WCT. Having a history of cardiovascular disease (i.e., myocardial infarction, coronary artery disease,
congestive heart failure) will predispose patients to have WCTs secondary to ventricular etiologies. A small
retrospective study concluded that there is a greater than 95% positive predictive value of VT for patients who had a
history of previous myocardial infarction, congestive heart failure, or a recent episode of chest pain.[6] Additionally,
physicians should thoroughly inquire about a patient’s medication history, particularly if they are taking any
antiarrhythmics. These medications are known to prolong the QRS complex (which can be misinterpreted as WCTs),
but more importantly and ironically, they can also cause arrhythmias. It is also imperative to ask patients if they have
a pacemaker or to identify it on a physical exam. If a patient with a known permanent pacemaker were to present with
a WCT, the device could be a cause of this arrhythmia and would change management/treatment.

Although subtle, a careful and scrupulous physical exam can strongly suggest the diagnosis of VT. During the
physical exam, the physician should focus on signs of atrioventricular dissociation, which includes: irregular cannon
A waves, changes in S1 heart sound, and labile systolic blood pressure with respect to heartbeats. All of these exam
findings occur during VT because they indicate that the atria and ventricles are functioning independently of one
another. It is important to know that the absence of these exam findings does not exclude VT as the cause of WCT, nor
does it confirm SVT as an etiology. Some physical exam maneuvers can be helpful in distinguishing between SVT
and VT. These are known as vagal maneuvers, which include: carotid sinus massage, Valsalva, coughing, breath
holding, squatting, water immersion, and many others. SVT responds to vagal maneuvers by slowing down the heart
rate and allowing atrial activity (p waves) to be easily seen. VT will typically not respond at all these maneuvers.[1]

Evaluation
Physicians should always remain vigilant when managing WCT as these patients can quickly become unstable and
experience sudden cardiovascular collapse. The EKG will be an essential diagnostic tool that will assist in diagnosing
the etiology of WCTs. A good rule of thumb is that any EKG with WCT is VT until proven otherwise. Rapidly and
accurately diagnosing WCT still remains a problem because there are numerous algorithms and complicated criteria
that can be difficult to remember in an emergency situation. Approximately 90% of WCTs can be diagnosed with
almost absolute certainty, but despite the availability of numerous algorithms and criteria available, 10% of cases are
still misdiagnosed. For the differentiation of WCTs, this article will review the most well-known approaches but will
not discuss them in detail, given that they are complicated, and its use would be challenging in an urgent setting.

Prior to the development of distinguished algorithms, WCTs were differentiated using the Traditional Criteria, which
was created through the contribution of several authors such as Sandler, Swanick, Marriott, Wellens, Coumel, and
Kindwall. The established subsequent step-wise algorithms would incorporate principles from the Traditional
Criteria as well as developing new ones. The most famous and commonly used algorithm to date is the Brugada
algorithm. Vereckei published two algorithms which proved to be superior to Brugada but were limited, given that
they were more time consuming compared to Brugada. The ACC (American College of Cardiology), AHA (American
Heart Association), and ESC (European Society of Cardiology) have developed an algorithm for the practical
approach and evaluation of WCTs in otherwise hemodynamically stable patients. Important things to keep in mind are
key aspects of the medical history (i.e., previous heart attack, history of congestive heart failure, chest pain, older age,
structural heart disease) and physical exam (i.e., signs of atrioventricular dissociation) that have been discussed
previously.

Morphology on EKG that is strongly suggestive for VT is AV dissociation, the finding of fusion beats and capture
beats which signify AV dissociation, extreme axis deviation (NW axis), initial R or Rs wave in limb lead aVR,
absence of RS complexes in precordial leads (leads V1-V6), positive or negative concordance across the precordial
leads, and an R wave peak time >50 ms in limb lead II. The diagnosis of SVT as the cause for WCT would be more
indicative if there is evidence of a typical BBB or fascicular block. Interestingly, if the QRS morphology during sinus
rhythm is similar to the QRS morphology during an episode of WCT, this can either be SVT or VT. VT will usually
be a regular rhythm depending on the timing of the WCT episode, history of anti-arrhythmic medication use, and
history (or undiagnosed) focal idiopathic VT. Also, if a WCT appears to have an irregular rhythm, caution should be
advised as the underlying etiology could be Afib with WPWS (or Afib with aberrancy), and mismanagement could
lead to serious consequences. In concordance with EKGs, exam maneuvers can be helpful in distinguishing between
SVT and VT. Vagal maneuvers (i.e., carotid sinus massage, Valsalva, coughing, etc.) cause an increase in
parasympathetic tone/response, which would normally lower one’s heart rate. Tachycardia, which is resolved by vagal
maneuvers, is most likely to be SVT. WCT caused by VT is typically known to not resolve with vagal maneuvers.
However, interestingly enough, idiopathic outflow tract VT can be terminated from these maneuvers.[2][7][8][2]

Treatment / Management
Physicians must act quickly and determine whether a patient is stable or unstable when during their initial evaluation
of WCT. It is critical to first evaluate both the patient’s ABCs (airway, breathing, circulation) and hemodynamic status
because it will guide your management in the emergency setting. If the patient is unresponsive, not protecting their
airway, or not breathing (but has a pulse) then they should be immediately intubated in order to secure their airway. If
a patient has low oxygen saturation on the pulse ox, then supplemental oxygen should be initiated. If a patient does
not have a pulse, immediately begin chest compressions and follow ACLS protocol guidelines. Intravenous access,
EKG, cardiac rhythm monitoring, and blood pressure monitoring should be started immediately on all patients who
complain of chest discomfort. Once a hemodynamically unstable patient is found to have a WCT, emergent
cardioversion (or defibrillation) should be your next immediate step as it will reduce morbidity and mortality. It is
critical to know how to cardiovert an unstable patient as these two methods of delivering electrical shocks are quite
different. The presence or absence of an unstable patient’s pulse is what determines which type of cardioversion will
be used. If the patient has a pulse, then synchronized cardioversion will be preferred as it will be coordinated with the
heart’s electrical activity (QRS complex) to reduce the risk of inducing cardiac arrest. If the patient does not have a
pulse, then this will be considered a cardiac arrest and requires immediate defibrillation.[9][10]

In stable patients, pharmacologic treatment should be based on the most updated AHA ACLS guideline along with
cardioversion. Below you will find a modified algorithm from AHA guidelines for the emergency management and
resuscitation of hemodynamically unstable patients presenting with WCT. It is important to always consider reversible
causes (i.e. acute ischemia, myocardial infarction, electrolyte abnormalities, drug toxicities) in unstable patients
because some can be easily corrected. As mentioned previously, if uncertain regarding the etiology of WCT, it is
better to err on the side of caution and treat arrhythmia as VT given that it is the most common cause and has more
detrimental consequences if managed inappropriately. During the emergent setting, it is necessary to stabilize the
patient, treat any reversible causes, and leave the process of refining the diagnosis once the patient is admitted and
stable.

When considering a pharmacologic intervention, it is important to have some clinical suspicion about whether the
origin of the WCT is coming from the atria or the ventricles.

SVT will typically be managed with adenosine, Afib with WPWS will be treated with amiodarone, and Afib
with aberrancy with either diltiazem or a beta-blocker.

Typically, amiodarone will be the first-line drug of choice for all ventricular arrhythmias (VT, polymorphic VT,
Vfib, etc.) Lidocaine can also be considered as a potential 2nd line medication but it should never be used for
WCT of unknown origin.

If the EKG shows evidence of Torsades de Pointes, then it is essential to give magnesium as this will be the
most effective way to treat this ventricular arrhythmia. If Torsades is refractory to magnesium, one could
perform overdrive pacing (heart rate of 90 to 130 bpm) which is generally successful in these circumstances.

If a patient is clinically stable and time permits, knowing the cause of their WCT will allow the physician to correctly
treat/manage the etiology and further reduce the potential risk for morbidity and mortality. For example, VT (with
pulses) is normally treated with either anti-arrhythmic medications or electrical cardioversion. If one were to mistake
Afib for VT and treat with electrical cardioversion, this could have some serious consequences. When the atria beat
irregularly/spastically, this increases the risk of clot formation on the atrial walls. A patient who is not anti-coagulated
and was to receive cardioversion in the setting of Afib, their risk of possible stroke will be 1.5% due to clot
dislodgement.[11] Another example is mistaking VT for SVT. As stated previously, SVT can be managed
conservatively with vagal maneuvers or with medications (i.e. adenosine, diltiazem, verapamil). Adenosine effectively
resolves tachycardia caused by SVT by blocking electrical conduction through the AV node. Giving adenosine in VT
can effectively slow the rate which can aid in diagnosis and in some rare instances, can cardiovert.[12][13]

One of the most important factors to consider when administering pharmacologic treatment for WCT is the possibility
that a patient may have an alternative conduction pathway that is atypical of normal cardiac anatomy. These
alternative pathways can either be outside of the AV node or within the AV node. These alternative pathways are
problematic due to their faster electrical conduction velocities compared to the AV node. When these pathways are
used, they result in faster activation of the ventricular myocardium and can create a positive feedback loop and lead to
very high ventricular rates. The complications of these pathways could be potentiated by AV nodal blockade
medications (i.e. adenosine, calcium channel blockers, and beta-blockers).

Erroneously giving adenosine in irregular WCT (or when there is a concern for an aberrant pathway) can cause
coronary ischemia or precipitate dangerous arrhythmias such as Afib with RVR (rapid ventricular response), Vfib, or
torsades de pointes.[3][5][14] With respect to calcium channel blockers (i.e. diltiazem and verapamil), these
medications weaken the strength of cardiac contractions (negative ionotropy) and slow down the electrical conduction
via the AV node. If a patient has an alternative conduction pathway, complications from these medications result in the
use use of aberrant pathways which can lead to significant hemodynamic collapse from profound vasodilation,
increased rate of VT, or degeneration to Vfib.

Patients with a known permanent pacemaker who presents with a WCT, the device should be considered as a potential
cause of arrhythmia and would be managed differently. A magnet would be placed directly over the pacemaker and
would likely terminate this arrhythmia. The magnet works by disabling the pacemaker’s atrial sensing capability and
essentially reprograms it to an asynchronous form of pacing.[1][2][15]

Differential Diagnosis
Below is a broad differential diagnosis for WCT, which also consists of potential etiologies.[1][2]

Supraventricular tachycardia (SVT) with pre-existing bundle branch block (BBB)

SVT with rate-related BBB

SVT with aberrant conduction

Atrial fibrillation (Afib) with Wolff-Parkinson-White syndrome (WPWS)

Ventricular tachycardia (VT)

Ventricular fibrillation (VFib)

Polymorphic VT (torsades de pointes)

Pacemaker mediated tachycardia (PMT)

Drug overdose (i.e., TCA’s, digitalis, cocaine, lithium, diphenhydramine)

Sodium channel blockers

Hyperkalemia

Hyper or hypo-magnesemia

Post-resuscitation (ROSC)

EKG artifact

Genetic disorders

Long QT syndrome

Short QT syndrome

Hypertrophic cardiomyopathy
 Familial dilated cardiomyopathy

Brugada syndrome

Catecholaminergic polymorphic ventricular tachycardia

Arrhythmogenic right ventricular dysplasia

Prognosis
Although there is a wide differential for the causes of WCT, the prognosis of all these etiologies is dependent on the
duration of the arrhythmia, how it affected the hemodynamic stability of the patient during the episode, and if the
patient had any subsequent complications from the event. Patients who are hemodynamically stable on initial
presentation and their WCT is quickly terminated typically tend to have a better prognosis than those who are unstable
because of the lower incidence of complications. Prognosis is also dependent on preventing the recurrence of WCT.
Patients with a history of VT (or at increased risk for it) may be eligible for placement of implantable cardioverter-
defibrillator (ICD) devices, which can help improve morbidity and mortality. Catheter ablation is also another
potential treatment option for some etiologies of WCT, which can improve prognosis. Myocardial infarction is a
potential complication during a WCT event, which can further worsen a patient’s prognosis due to the increased risk
for sudden death. Left ventricular ejection fraction (LVEF) is strongly associated with a patient’s prognosis and can
help determine those who are at risk for sudden cardiac death. Patients with an LVEF of < 30% are considered to have
an overall annual mortality rate that approaches 10%.[2][15]

Complications
VT is the most common cause of WCT, and the severity of its complications is determined by the duration and
frequency of the arrhythmia and predisposing risk factors. VT most commonly occurs in patients with a history of
cardiovascular disease (i.e., coronary artery disease, myocardial infarctions, structural heart disease). Common
complications of VT include frequent episodes of syncope (and associated physical injuries sustained during the
syncopal event) as well as decreased efficiency of the heart to pump blood, which could lead to heart failure.
Although a history of cardiovascular disease poses its own risk for complications, this, in conjunction with VT, has
increased risk for the most feared complication - sudden cardiac death. This fatal complication is defined as a death
that occurs unexpectedly, immediately or an abrupt change in a patient’s clinical presentation within one hour from
the onset. Sudden cardiac death is believed to be secondary to VT deteriorating to the lethal Vfib arrhythmia.

In the United States, sudden cardiac death consists of 15% of the total causes of mortality and greater than half of all
cardiac-related deaths. It is also important to keep in mind that a small portion of sudden cardiac deaths are from
inherited familial disorders and should be carefully evaluated in patients with family members who were young, and
died suddenly/unexpectedly.[15]

Deterrence and Patient Education

Cardiovascular disease is the utmost important predisposing risk factor for the most common cause of WCT.
Therefore, to effectively combat and prevent VT, one should reduce the risk of developing any form of heart disease
by adopting healthier lifestyle modifications. These include exercise regularly, a healthy diet, weight loss, manage
stress appropriately, smoking cessation, limit alcohol intake, and avoid illicit drug use (i.e., cocaine). For those who
already have a diagnosis of cardiovascular disease, the best way to prevent VT is to follow up regularly with your
primary care doctor, take your medications as instructed, monitor your blood pressure, keep glucose and cholesterol
levels under control, and adopt lifestyle modifications. Although it occurs infrequently, there is a form of VT (i.e.,
idiopathic VT) that can result from someone without any prior history of heart disease.[16]

Enhancing Healthcare Team Outcomes

Although the management of WCT is complex, given its broad differential and numerous etiologies, this article
emphasizes a multidisciplinary team approach for ventricular arrhythmias because they are the most common cause of
WCT. A multidisciplinary team will be required during both the in-patient and outpatient setting.
This team usually consists of emergency room physicians, cardiologists, cardiac electrophysiologists, ICU
intensivists, clinical pharmacists, nurses, nutrition specialists, case managers, cardiac rehabilitation specialists,
psychologists, and primary care physicians. It is beneficial to have multiple team members involved as it can optimize
a patient’s care and improve their quality of life. Typically while the patient is in the hospital, their care is
predominantly coordinated by the primary cardiologist in conjunction with a cardiac electrophysiologist who will
decide on optimal treatment options taking into consideration the patient’s risk factors and comorbidities. Once these
patients are discharged home from either the hospital or rehabilitation centers, they will still require a
multidisciplinary approach to facilitate their care.

In the outpatient setting, the patient’s care is usually managed by both their primary care doctor and cardiologist.
Those patients who are treated with implantable devices or defibrillators may encounter repetitive shocks if they have
recurrent ventricular arrhythmias. In return, being repeatedly shocked can reduce a patient’s quality of life by
inducing significant anxiety. It is important to keep in mind that these patients should also have some form of
psychological support upon discharge into the community.[17][18]

Review Questions

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Comment on this article.

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Disclosure: Manuel Obando declares no relevant financial relationships with ineligible companies.

Disclosure: Erin Marra declares no relevant financial relationships with ineligible companies.

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