Wide QRS complex tachycardias: Approach to management

INTRODUCTION — Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG).

●A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the atrioventricular (AV) node (ie, a supraventricular tachycardia [SVT]).

●A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow for one of the following reasons (see "Wide QRS complex tachycardias: Causes, epidemiology, and clinical manifestations", section on 'Differential diagnosis of WCT'):

•The arrhythmia originates outside of the normal conduction system (ie, ventricular tachycardia [VT])

•Abnormalities within the His-Purkinje system (ie, SVT with aberrancy)

•Pre-excitation with an SVT conducting antegrade over an accessory pathway, resulting in direct activation of the ventricular myocardium

A wide complex tachycardia (WCT) represents a unique clinical challenge for two reasons:

●Diagnosing the arrhythmia is difficult – Although most WCTs are due to VT, the differential diagnosis includes a variety of SVTs (algorithm 1). Diagnostic algorithms to differentiate these two etiologies are complex and imperfect.

●Urgent therapy is often required – Patients may be unstable at the onset of the arrhythmia or deteriorate rapidly at any time, particularly if the WCT is VT [1-4].

The management of patients with a wide QRS complex tachycardia will be discussed here. The clinical manifestations, diagnosis, and initial evaluation of patients with a wide QRS complex tachycardia, as well as discussion of narrow QRS complex tachycardias, is presented separately. (See "Wide QRS complex tachycardias: Approach to the diagnosis" and "Overview of the acute management of tachyarrhythmias" and "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy" and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation".)

MANAGEMENT — The acute management of a patient with WCT depends on the hemodynamic stability of the patient [5]. Urgent or emergency management is required in unstable patients, with management taking precedence over further diagnostic workup until the patient has been stabilized. Following initial management and stabilization of the patient, chronic management of the patient with WCT will be directed by the etiology of the WCT (supraventricular versus ventricular).

Initial management — All patients with a WCT should have a brief immediate assessment of the symptoms, vital signs, and level of consciousness to determine if they are hemodynamic stable or unstable. While the assessment of hemodynamic status is being performed by a clinician, other members of the health care team should:

●Administer supplemental oxygen

●Establish intravenous access

●Send blood for appropriate initial studies (see "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'Ancillary testing')

●Attach the patient to a continuous cardiac monitor

●Obtain a 12-lead ECG

Differentiation between a hemodynamically stable versus unstable patient is as follows (see "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'Assessment of hemodynamic stability'):

●An unstable patient will have evidence of hemodynamic compromise, such as hypotension, altered mental status, chest pain, or heart failure, but generally remains awake with a discernible pulse. Patients who become unresponsive or pulseless are considered to have a cardiac arrest and are treated according to standard resuscitation algorithms.

●A stable patient shows no evidence of hemodynamic compromise despite a sustained rapid heart rate, but should have continuous monitoring and frequent reevaluations due to the potential for rapid deterioration as long as the WCT persists.

Patients who are initially stable may rapidly become unstable, particularly in the setting of extremely rapid heart rates (greater than 200 beats per minute) or significant underlying cardiac comorbidities.

Unstable patients — Hemodynamic compromise may occur with any WCT, regardless of the etiology, but is more likely in patients with ventricular tachycardia (VT). Patients who are felt to be hemodynamically unstable require prompt treatment with electrical cardioversion/defibrillation to prevent further clinical deterioration or sudden cardiac arrest (SCA).

●Patients with WCT who are hemodynamically unstable and pulseless, or who become pulseless during the course of evaluation and treatment, should be managed according to standard advance cardiac life support (ACLS) resuscitation algorithms, with immediate high-energy countershock and cardiopulmonary resuscitation (CPR) (algorithm 2). Patients should initially be treated with a synchronized (if possible) 120 to 200 joule shock from a biphasic defibrillator or a 360 joule shock from a monophasic defibrillator; if synchronization is not possible, then an unsynchronized countershock should be delivered, typically at higher energy doses [6]. (See "Advanced cardiac life support (ACLS) in adults" and "Adult basic life support (BLS) for health care providers" and "Supportive data for advanced cardiac life support in adults with sudden cardiac arrest".)

●For patients with WCT who are hemodynamically unstable, but still responsive with a discernible blood pressure and pulse, we recommend urgent cardioversion (with procedural sedation when feasible). The selection of energy level and the choice between synchronized and unsynchronized shocks depends on the clinical situation (algorithm 3):

•If the QRS complex and T wave can be distinguished, an attempt at emergent synchronized cardioversion can be performed. Initial cardioversion is performed with a synchronized shock of 100 joules using either a biphasic or monophasic defibrillator, with upward titration of the energy if additional shocks are needed [6].

•If the QRS complex and T wave cannot be distinguished accurately, a synchronized shock is not possible. Patients should initially be treated with an unsynchronized 120 to 200 joule shock from a biphasic defibrillator or a 360 joule shock from a monophasic defibrillator [6].

•Intravenous analgesics or sedatives should be cautiously administered if the blood pressure will tolerate their use. However, the use of such agents must be balanced against the risks of further hemodynamic deterioration, and therapy should not be unnecessarily delayed if the ability to administer conscious sedation is not readily available.

Stable patients with uncertain WCT etiology — In a patient with WCT who is hemodynamically stable, additional time may be spent attempting to determine the diagnosis. If the initial diagnosis of WCT was made from a single-lead rhythm strip, a full 12-lead ECG should be obtained during the WCT and methodically reviewed as this may provide additional clues to the etiology. In addition, a trial of vagal maneuvers and/or pharmacologic intervention can provide both diagnostic information and, on occasion, prove therapeutic if there is resolution of the WCT. (See "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'Evaluation of the electrocardiogram'.)

For hemodynamically stable patients with WCT which is regular and monomorphic in whom the etiology of the WCT remains uncertain, we suggest the following approach (algorithm 3):

●Perform vagal maneuvers (Valsalva, carotid sinus massage, etc) – Introducing transient block at the AV node can serve as a diagnostic/therapeutic challenge. Most supraventricular tachycardias (SVTs) are AV node dependent (eg, atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia [AVRT]), so transient AV nodal block will terminate most SVTs. Atrial flutter and atrial tachycardia may be "unmasked" by transient AVN block. Vagal maneuvers should have no significant effect on VT. (See "Vagal maneuvers".)

●Administer adenosine – Intravenous adenosine has essentially the same effect as vagal maneuvers on SVT and atrial flutter/tachycardia. Some idiopathic VTs (eg, right ventricular outflow tract [RVOT] VT) may terminate with adenosine. Resuscitation equipment should be immediately available as rarely adenosine will precipitate hemodynamic collapse. The initial dose of adenosine is 6 mg; if this has no effect, 12 mg can be administered.

●Avoidance of other pharmacologic agents – Intravenous beta blockers, calcium channel blockers, and digoxin are not typically used, due to the potential for hemodynamic deterioration (often the result of hypotension) in patients with a previously stable WCT.

●Further treatment is directed by the response to vagal maneuvers and/or adenosine, specifically targeting VT or the relevant SVT. If the WCT persists and the etiology remains uncertain, we proceed as though the WCT is VT and treat accordingly. (See 'Stable patients with known WCT etiology' below.)

While any ECG analysis and diagnostic/therapeutic maneuvers are being performed, close observation and continuous ECG monitoring are paramount, as patients with WCT who appear stable initially may experience a rapid deterioration of their clinical status with little or no warning.

Vagal maneuvers — In patients with WCT of uncertain etiology, the response to vagal maneuvers may provide insight to the mechanism responsible for the arrhythmia. We perform one or more vagal maneuvers in all patients with WCT who are hemodynamically stable, often while preparing for pharmaceutical therapy or cardioversion. However, these interventions are associated with some risk, primarily the potential for hemodynamic deterioration in a borderline unstable patient, and as such should only be performed by experienced individuals in an environment capable of dealing with potential sequelae.

Vagal maneuvers increase parasympathetic input to the heart, which slows the rate of sinus node impulse formation and slows AV node conduction velocity while simultaneously lengthening the refractory period. The Valsalva maneuver and carotid sinus massage, two of the most commonly performed vagal maneuvers which enhance vagal tone and therefore depresses sinus and AV nodal activity, can be easily and quickly done at the bedside. (See "Vagal maneuvers".)

Examples of how various arrhythmias respond to vagal stimulation include (see "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Possible outcomes following vagal maneuvers or adenosine administration'):

●Sinus tachycardia will gradually slow during the maneuver and then accelerate upon completion of the maneuver.

●During atrial tachycardia or atrial flutter, the ventricular response will transiently slow (due to increased AV nodal blockade). The arrhythmia itself, which occurs within the atria, is usually unaffected.

●A paroxysmal SVT (either atrioventricular nodal reentrant tachycardia [AVNRT] or AVRT) will frequently terminate because of the dependence on the AV node.

●VT is generally unaffected by vagal maneuvers, although these maneuvers may slow or block retrograde conduction. In some cases, this response exposes AV dissociation by altering the sinus rate (or PP intervals). Rarely, VT terminates in response to carotid sinus pressure.

Pharmacologic interventions — In patients with WCT of uncertain etiology, the response to the administration of certain drugs can provide diagnostic information, which in certain circumstances may also provide a therapeutic benefit (eg, adenosine which may terminate some SVTs) [5]. However, some drugs used for the diagnosis or treatment of SVT (eg, verapamil, adenosine, or beta blockers) can cause severe hemodynamic deterioration (often the result of hypotension) in patients with a previously stable VT, potentially resulting in ventricular fibrillation (VF) and cardiac arrest [1-3]. Thus, other than adenosine, these medications are generally reserved for the treatment of patients in whom the diagnosis of SVT is already known; they are rarely used for diagnostic purposes for a WCT. (See 'Supraventricular tachycardia' below.)

Adenosine slows conduction time through the AV node. Arrhythmias that are dependent upon the AV node (eg, AVNRT, AVRT) will frequently be terminated following adenosine administration. Adenosine will usually not terminate other non-AV node dependent arrhythmias; a subgroup of atrial tachycardias may be adenosine sensitive. In addition, some idiopathic VTs (specifically RV outflow tract VT) may terminate with adenosine. If the tachycardia does not terminate, the ventricular response following adenosine administration is often helpful in distinguishing the etiology of the WCT. Not infrequently, adenosine will promote the conversion of SVT to atrial fibrillation (AF). If the patient has underlying Wolff-Parkinson-White (WPW) syndrome, this may lead to extremely rapid ventricular rates, and potentially deterioration to VF. Thus, an external defibrillator should always be available. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Possible outcomes following vagal maneuvers or adenosine administration'.)

●If there is no change in the ventricular rate and rhythm, the WCT is likely VT. One exception would be if the adenosine was not properly administered (ie, rapid intravenous push followed by saline flush) and, because of its short half-life and metabolism by red blood cells, did not reach the heart.

●If the ventricular activity temporarily slows or ceases (for 5 to 10 seconds), the remaining atrial activity is typically easily seen on the ECG and can be analyzed to determine the etiology of WCT. A second dose of 12 mg of adenosine, although appropriate for the treatment of known SVT, is probably not appropriate for WCT that is not known to be SVT.

Adenosine is administered via rapid intravenous push, followed immediately by 10 mL saline flush. Common side effects include facial flushing, shortness of breath, palpitations, chest pain, and lightheadedness. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Administration and side effects'.)

Stable patients with known WCT etiology — In a patient with WCT who is hemodynamically stable, therapy may be targeted to the specific arrhythmia (VT or SVT) when identifiable from the available data. (See "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'ECG initial impressions'.)

●VT should be suspected in patients with clearly identified AV dissociation, patients with QRS concordance and a right superior axis (or axis shift of greater than 40 degrees from baseline), and in patients with known structural heart disease. VT is typically regular, though slight variation of the RR interval may be seen.

●SVT should be suspected in young patients with structurally normal hearts in whom none of the historical (eg, family history of sudden cardiac death), physical, or ECG criteria supporting VT are present, or in patients with a history of SVT with a similar presentation. The RR interval in SVT is generally very regular.

●Significant irregularity in a WCT is most often seen in patients with AF and aberrant conduction, though polymorphic VT is also irregular. Patients with AF should have similar QRS morphologies for every beat, while the QRS morphology varies in polymorphic VT. An important exception is pre-excited AF in patients with WPW syndrome, in which the QRS morphology is variable in width and morphology. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Atrial fibrillation'.)

Ventricular tachycardia — Once the WCT has been established as VT, therapy should be promptly provided. Patients with VT who are hemodynamically stable may remain stable or may become unstable rapidly and without warning. The choice of initial treatments for hemodynamically stable VT includes electrical or pharmacologic cardioversion. Some of our experts proceed directly to electrical cardioversion, while others prefer to begin with an intravenous antiarrhythmic agent and reserve cardioversion for refractory patients or for those who become unstable.

●If electrical cardioversion with appropriate procedural sedation is the chosen approach, intravenous analgesics or sedatives should be cautiously administered if the blood pressure will tolerate their use. If the QRS complex and T wave can be distinguished, an attempt at emergent synchronized cardioversion can be performed with a synchronized shock of 100 joules using either a biphasic or monophasic defibrillator. If the QRS complex and T wave cannot be distinguished accurately, and a synchronized shock is not possible, we administer an unsynchronized 120 to 200 joule shock from a biphasic defibrillator or a 360 joule shock from a monophasic defibrillator.

●If pharmacologic cardioversion is the chosen approach, we administer intravenous amiodarone (150 mg IV over 10 minutes, followed by 1 mg/minute for the next six hours) or procainamide (20 to 50 mg per minute until arrhythmia terminates or a maximum dose of 15 mg/kg is administered) (algorithm 4). Often administration of these drugs may result in hypotension, which may hasten the need for electrical cardioversion. (See 'Recurrent or refractory WCT' below.)

●Any associated conditions should be treated, including cardiac ischemia, heart failure, electrolyte abnormalities, or drug toxicities.

●For patients with one of the known syndromes of VT in structurally normal hearts, calcium channel blockers or beta blockers may be used, particularly if the patient has been successfully treated in the past with such medications. These drugs can be used either to terminate the arrhythmia, or after cardioversion to suppress recurrences. (See "Ventricular tachycardia in the absence of apparent structural heart disease".)

Given the risk for hemodynamic deterioration at any time, an external defibrillator should be immediately available at all times prior to and during the administration of any antiarrhythmic drugs.

Supraventricular tachycardia — Once the WCT has been definitively established as SVT, therapy directed at the SVT may be given. In such cases, management is similar to an SVT with a normal QRS duration [5]. The ECG recording when the tachycardia slows or terminates can provide valuable information for diagnosing the specific type of SVT. Thus, in a stable patient, a continuous rhythm strip, preferably a 12-lead rhythm strip, should be recorded during any intervention intended to terminate the arrhythmia or slow the ventricular response.

For patients with known SVT, we suggest the following approach:

●If the SVT is likely to be AVNRT or AVRT, or if the specific SVT diagnosis is uncertain, the following treatments are recommended:

•Vagal maneuvers – We recommend Valsalva maneuver or carotid sinus pressure (if no carotid bruits are present) as the initial intervention, given the ease with which this can be rapidly performed at the bedside.

•Adenosine – For patients with persistent SVT following vagal maneuvers, adenosine is highly effective in terminating many SVTs (eg, AVNRT, AVRT), and for others (eg, AF, atrial flutter), adenosine may facilitate the diagnosis by slowing the ventricular response to allow clearer assessment of atrial activity [7]. Adenosine dosing is discussed in an algorithm (algorithm 5). (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Administration and side effects'.)

•Calcium channel blockers or beta blockers – If SVT persists after vagal maneuvers and adenosine administration, the choice of initial pharmacologic therapies includes non-dihydropyridine calcium channel blockers and beta blockers. We generally start with intravenous verapamil (5 to 10 mg IV bolus over two minutes; if no response, an additional 10 mg IV bolus may be administered 15 to 30 minutes following the initial dose) or diltiazem (15 to 20 mg IV), although a beta blocker (eg, metoprolol 2.5 to 5 mg IV bolus over two to five minutes; if no response, additional 2.5 to 5 mg IV boluses may be given to a total dose of 15 mg over 15 minutes) may be given. These medications can terminate AVNRT or AVRT, as well as some atrial tachycardias. If the specific SVT diagnosis remains unknown, these drugs may slow the ventricular response and facilitate diagnosis.

•Cardioversion – Electrical cardioversion is rarely necessary in patients with a stable SVT. However, if WCT persist after the above interventions, synchronized cardioversion is usually effective in restoring sinus rhythm. Following appropriate procedural sedation, an initial synchronized shock of 100 to 200 joules (monophasic) or 50 to 100 joules (biphasic) is administered.

●If the arrhythmia is known to be atrial fibrillation, atrial flutter, or an atrial tachycardia, management options include rate control and cardioversion (ie, rhythm control). Decisions regarding which strategy is appropriate in a given patient are addressed separately. (See "Overview of atrial flutter" and "Atrial fibrillation: Overview and management of new-onset atrial fibrillation".)

After the WCT is terminated or controlled, the further management of an SVT depends upon which SVT is present. (See "Atrioventricular nodal reentrant tachycardia" and "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway".)

Patients with a pacemaker — Patients with a permanent pacemaker are subject to the same array of WCTs as patients without a pacemaker. Rarely, however, WCT can result from a pacemaker tracking an underlying atrial arrhythmia or be due to pacemaker-mediated tachycardia. Most patients with WCT involving a pacemaker will be hemodynamically stable, unless the resulting tachycardia exacerbated underlying comorbidities (eg, angina, heart failure, etc).

If the WCT is thought to be directly related to the function of the pacemaker, the appropriate therapy is the placement of a magnet over the pacemaker. The magnet will disable all pacemaker sensing, thereby terminating the ability of the pacemaker to track atrial impulses. With the magnet, the pacemaker will function in an asynchronous, fixed-rate mode (ie, VOO or DOO). In this situation, there will be pacemaker stimuli that do not sense the P wave or QRS complex and will occur with a fixed rate (ie, the lower rate limit of the pacemaker). If WCT is due to pacemaker-mediated tachycardia (PMT) or "pseudo PMT" (non-reentrant repetitive VA synchrony), transient magnet application will terminate the WCT, and the underlying rhythm (with pacing, if appropriate) will ensue when the magnet is removed. If the WCT is due to inappropriate tracking of atrial fibrillation or atrial flutter, the WCT will likely resume once the magnet is removed.

Patients with pacemakers may also be subject to WCTs that do not involve the pacemaker, like other patients. In stable patients, the pacemaker programmer can be used to telemeter the intracardiac electrograms from the pacemaker leads. Examination of these electrograms may yield the diagnosis, as in the electrophysiology laboratory.

Patients with an ICD — Patients with an implantable cardioverter-defibrillator (ICD) represent a specific high-risk population in whom WCT is far more likely to represent VT. Patients who underwent ICD implantation for secondary prevention have previously experienced a sustained ventricular tachyarrhythmia or sudden cardiac death, while those who received an ICD for primary prevention were felt to be at increased risk of sustained ventricular tachyarrhythmia. In either case, WCT in patients with an ICD should be treated as VT until proven otherwise. When no ICD therapy has been delivered, and the device cannot be immediately interrogated (due either to lack of equipment or personnel, or patient instability), the initial management should proceed as if no ICD were present.

The presence of an ICD has a number of unique implications for patients with a WCT. Although the ICD should be programmed to delivery therapies (either antitachycardia pacing or shocks) for a WCT, such therapies are usually delivered within the first minutes of the arrhythmia.

●In a patient with a persistent or recurrent WCT, the ICD may not always provide definitive management if the device has reached the limit of programmed therapies. Patients with a WCT which persists following multiple ICD therapies most likely have either VT storm with an underlying trigger (eg, ischemia, hypokalemia) or an SVT with aberrant conduction which recurs or persists in spite of the ICD therapies. (See "Electrical storm and incessant ventricular tachycardia".)

●Patients with and ICD and WCT will not receive therapy from the ICD if the WCT rate is lower than the programmed rate for ICD therapy.

●Patients with an ICD who receive multiple shocks but do not have a tachycardia most likely have device malfunction, usually related to lead malfunction. In these patients, magnet application can temporarily suspend tachycardia therapy and prevent further inappropriate shocks. Magnet application is also appropriate in patients receiving shocks for narrow complex tachyarrhythmias (SVT, AF, atrial flutter, sinus tachycardia). (See "Cardiac implantable electronic devices: Long-term complications".)

All modern ICDs also have the capacity to function as a pacemaker. Patients with a single lead ICD (typically an endovascular lead in the right ventricle) cannot sense and track atrial arrhythmias and, as such, are not subject to WCT associated with the device. Conversely, patients with both an atrial and a ventricular lead have the capacity to sense and track atrial arrhythmias and therefore can potentially develop WCT associated with the pacemaker. However, given the risk of WCT representing VT in a patient with an ICD, pacemaker-associated WCT should be considered only after exclusion of other WCT etiologies and following ICD interrogation. Magnet application does not force asynchronous pacing in ICDs and will therefore not terminate PMT in patients with ICDs. As in pacemaker patients, telemetered intracardiac recordings may be helpful diagnostically. (See 'Patients with a pacemaker' above.)

Recurrent or refractory WCT — If the WCT recurs or persists following initial attempts at vagal maneuvers, diagnostic pharmacologic interventions, and electrical cardioversion, suppression of the arrhythmia by pharmacologic means should be attempted and further evaluation should focus upon the presence of arrhythmia triggers (eg, ischemia, electrolyte abnormalities, and drug toxicity). Amiodarone is generally the most effective agent for treatment of recurrent or refractory WCT, particularly VT [6]. Cardioversion or defibrillation should be repeated as necessary in patients who are hemodynamically unstable. (See "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis".)

●For patients with recurrent VT or WCT of uncertain etiology, we suggest the following:

•Amiodarone is administered in most settings, due to its efficacy in the suppression of both atrial and ventricular arrhythmias. The initial dose is 150 mg IV over 10 minutes followed by an infusion of 1 mg/minute for six hours, then 0.5 mg/minute for an additional 18 hours or longer. Repeat amiodarone boluses can be administered if necessary.

•Procainamide is an alternative to amiodarone that also suppresses both SVTs and VT. The initial dose is 15 to 17 mg/kg administered as slow infusion over 25 to 30 minutes, followed by 1 to 4 mg/minute by continuous infusion (algorithm 4). In addition, because of its ability to suppress conduction over a bypass tract, procainamide is recommended if antidromic AVRT or an SVT conducting over a bypass tract is suspected. For pre-excited atrial fibrillation or atrial flutter, intravenous procainamide or ibutilide is recommended; amiodarone and AV nodal blocking agents are not recommended. (See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome".)

●For patients with a known SVT that recurs or persists, intravenous verapamil, diltiazem, or beta blockers may be used.

Multiple recurrences of WCT should raise concern about cardiac ischemia, hypokalemia, digitalis toxicity, and polymorphic VT with or without QT prolongation, all of which have specific appropriate therapy. (See "Overview of the acute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST-elevation acute coronary syndromes" and "Cardiac arrhythmias due to digoxin toxicity" and "Clinical manifestations and treatment of hypokalemia in adults", section on 'Treatment' and "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management".)

Chronic therapy — Chronic therapy for patients with WCT will be driven by the underlying etiology of the WCT.

●Patients with VT should generally undergo implantation of an ICD. Following ICD implantation, those patients with recurrent symptomatic VT, or those who have received multiple ICD therapies, may require adjunctive antiarrhythmic therapy in an effort to suppress recurrent VT. In some cases, radiofrequency catheter ablation may be an option to reduce the frequency of VT. An important exception is idiopathic VT, which is treated with ablation or pharmacologic therapy, not with ICD. (See "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis", section on 'Chronic therapy' and "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy", section on 'Other treatment options'.)

●The approach to patients with WCT due to an SVT will vary significantly depending upon the etiology of the SVT.

•Patients with AVNRT or AVRT associated with a concealed accessory pathway may require no therapy, may be able to self-terminate arrhythmias using vagal maneuvers, may be candidates for pharmacologic suppressive therapy, or may be effectively cured with catheter ablation. (See "Atrioventricular nodal reentrant tachycardia", section on 'Preventive therapy' and "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Treatment to prevent recurrent arrhythmias'.)

•Patients with AVRT associated with a manifest accessory pathway or pre-excited atrial fibrillation or atrial flutter (ie, patients with arrhythmias related to WPW) should undergo electrophysiology testing and catheter ablation of accessory pathway due to the small risk of sudden cardiac death in patients with symptomatic WPW syndrome. (See "Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome", section on 'Treatment to prevent recurrent arrhythmias'.)

•The approach to a patient with atrial fibrillation may include ventricular rate control, restoration of sinus rhythm, or catheter ablation. (See "Atrial fibrillation: Overview and management of new-onset atrial fibrillation".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Arrhythmias in adults" and "Society guideline links: Ventricular arrhythmias" and "Society guideline links: Cardiac implantable electronic devices" and "Society guideline links: Supraventricular arrhythmias".)

SUMMARY AND RECOMMENDATIONS

●The acute management of a patient with wide QRS complex tachycardia (WCT) depends on the hemodynamic stability of the patient. Urgent or emergency management is required in unstable patients, with management taking precedence over further diagnostic workup until the patient has been stabilized. Following initial management and stabilization of the patient, chronic management of the patient with WCT will be directed by the etiology of the WCT (supraventricular versus ventricular). (See 'Management' above.)

●All patients with a WCT should have a brief immediate assessment of the symptoms, vital signs, and level of consciousness to determine if they are hemodynamic stable or unstable. An unstable patient will have evidence of hemodynamic compromise, such as hypotension, altered mental status, chest pain, or heart failure, whereas a stable patient shows none of these despite a sustained rapid heart rate. (See 'Initial management' above.)

●While the assessment of hemodynamic status is being performed by a clinician, other members of the health care team should administer supplemental oxygen, establish intravenous access, send blood for appropriate initial studies, attach the patient to a continuous cardiac monitor, and obtain a 12-lead electrocardiogram (ECG). (See 'Initial management' above and "Wide QRS complex tachycardias: Approach to the diagnosis", section on 'Ancillary testing'.)

●Patients with WCT who are hemodynamically unstable and pulseless, or who become pulseless during the course of evaluation and treatment, should be managed according to standard advance cardiac life support (ACLS) resuscitation algorithms, with immediate high-energy defibrillation and cardiopulmonary resuscitation (CPR) (algorithm 2). Patients should initially be treated with a synchronized (if possible) 120 to 200 joule shock from a biphasic defibrillator or a 360 joule shock from a monophasic defibrillator. An unsynchronized shock should be delivered if synchronization is not possible [6]. (See 'Unstable patients' above and "Advanced cardiac life support (ACLS) in adults" and "Adult basic life support (BLS) for health care providers".)

●For patients with WCT who are hemodynamically unstable, but still responsive with a discernible blood pressure and pulse, we recommend urgent cardioversion (with procedural sedation when feasible) (Grade 1A). (See 'Unstable patients' above.)

•If the QRS complex and T wave can be distinguished, an attempt at emergency synchronized cardioversion can be performed with a synchronized shock of 100 joules using either a biphasic or monophasic defibrillator.

•If the QRS complex and T wave cannot be distinguished accurately, and a synchronized shock is not possible, we administer an unsynchronized 120 to 200 joule shock from a biphasic defibrillator or a 360 joule shock from a monophasic defibrillator.

●For hemodynamically stable patients with WCT which is regular and monomorphic in whom the etiology of the WCT remains uncertain, we suggest vagal maneuvers (ie, Valsalva, carotid sinus massage) followed by intravenous adenosine if no response to the vagal maneuvers (Grade 2C). Further treatment is directed by the response to vagal maneuvers and/or adenosine, specifically targeting ventricular tachycardia (VT) or the relevant supraventricular tachycardia (SVT) (algorithm 5). If the WCT persists and the etiology remains uncertain, we proceed as though the WCT is VT and treat accordingly. (See 'Stable patients with uncertain WCT etiology' above.)

●For patients who are hemodynamically stable and known to have VT, some of our experts proceed directly to electrical cardioversion, while others prefer to begin with an intravenous antiarrhythmic agent (algorithm 4) and reserve cardioversion for refractory patients or for those who become unstable. (See 'Ventricular tachycardia' above.)

●For patients who are hemodynamically stable and known to have SVT, we suggest the following approach (Grade 2C) (see 'Supraventricular tachycardia' above):

•If the SVT is likely to be atrioventricular nodal reentrant tachycardia (AVNRT) or atrioventricular reciprocating tachycardia (AVRT), we perform vagal maneuvers, followed by adenosine, followed by intravenous verapamil or diltiazem, and, in refractory cases, electrical cardioversion. If the SVT terminates after any of the interventions, the subsequent interventions are not performed acutely.

•If the arrhythmia is known to be atrial fibrillation (AF), atrial flutter, or an atrial tachycardia, management options include rate control and cardioversion (ie, rhythm control). (See "Overview of atrial flutter" and "Atrial fibrillation: Overview and management of new-onset atrial fibrillation".)

●If the WCT is thought to be directly related to the function of pacemaker, the appropriate therapy is the placement of a magnet over the pacemaker. (See 'Patients with a pacemaker' above.)

●Chronic therapy for patients with WCT will be driven by the underlying etiology of the WCT, with patients having VT generally considered for implantable cardioverter-defibrillator (ICD) implantation, while therapy for patients with SVT will need to be tailored to the underlying arrhythmia. (See 'Chronic therapy' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Leonard Ganz, MD, FHRS, FACC, who contributed to an earlier version of this topic review.