Approach to the diagnosis of wide QRS complex tachycardias

Approach to the diagnosis of wide QRS complex tachycardias

Author:

Leonard I Ganz, MD, FHRS, FACC

Section Editors:

Peter J Zimetbaum, MD

Ary L Goldberger, MD

James Hoekstra, MD

Deputy Editor:

Brian C Downey, MD, FACC

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Oct 2017. | This topic last updated: Oct 22, 2015.

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

●A narrow QRS complex (<120 msec) 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 msec) occurs when ventricular activation is abnormally slow for one of the following reasons (see ‘Causes of WCT’below):

•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 a 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 ventricular tachycardia (VT), the differential diagnosis includes a variety of SVTs. 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 clinical manifestations, diagnosis, and initial evaluation of patients with a wide QRS complex tachycardia will be discussed here. The management of wide QRS complex tachycardias, as well as discussion of narrow QRS complex tachycardias, is presented separately. (See “Approach to the management of wide QRS complex tachycardias” and “Overview of the acute management of tachyarrhythmias” and “Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy” and “Clinical manifestations, diagnosis, and evaluation of narrow QRS complex tachycardias”.)

INITIAL APPROACH — The first priority when evaluating a patient with a wide complex tachycardia (WCT) is an assessment of patient stability. Unstable patients should be treated immediately, before an extensive diagnostic evaluation. (See ‘Assessment of stability’ below and “Approach to the management of wide QRS complex tachycardias”, section on ‘Unstable patients’.)

Stable patients will most often have already had an electrocardiogram (ECG) showing the presence of a WCT. In a stable patient, the ECG should be thoroughly and systematically reviewed in an effort to determine the etiology of the WCT. (See ‘Evaluation of the electrocardiogram’ below.)

In a stable patient, a focused clinical evaluation should include the following:

●History

●Physical examination

●Laboratory testing

●Diagnostic maneuvers in selected patients

The primary goals of the initial evaluation of a stable patient with WCT are to determine the etiology of the WCT (through evaluation of the ECG) and to elucidate any underlying conditions related to the event (eg, heart failure, myocardial ischemia, drug reaction, or electrolyte abnormalities). (See ‘Evaluation of the electrocardiogram’ below.)

Assessment of stability — Immediate assessments of the patient’s symptoms, vital signs, and the level of consciousness are of primary importance [5]. In the discussions that follow, patients are categorized as follows:

●Unstable – An unstable patient with WCT 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. In this setting, emergency synchronized cardioversion is the treatment of choice regardless of the mechanism of the arrhythmia. (See “Approach to the management of wide QRS complex tachycardias”, section on ‘Unstable patients’.)

Patients who become unresponsive or pulseless are considered to have a cardiac arrest and are treated according to standard resuscitation algorithms. (See “Advanced cardiac life support (ACLS) in adults” and “Basic life support (BLS) in adults”.)

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

The presence of hemodynamic stability should not be regarded as diagnostic of supraventricular tachycardia (SVT) [4,6]. Misdiagnosis of ventricular tachycardia (VT) as SVT based upon hemodynamic stability is a common error that can lead to inappropriate and potentially dangerous therapy [3,4]. (See “Approach to the management of wide QRS complex tachycardias”, section on ‘Pharmacologic interventions’.)

History — When evaluating the stable patient with a WCT, the following historical features may help determine the likely etiology and/or guide therapy:

●History of heart disease – The presence of structural heart disease, especially coronary heart disease and/or a previous myocardial infarction, strongly suggests VT as an etiology [4,7]. It is also important to establish whether a cardiac arrhythmia has occurred in the past and, if so, whether the patient is aware of the etiology. (See ‘Epidemiology’ below.)

●Presence of an implantable cardioverter defibrillator (ICD) – The presence of an ICD implies a known increased risk of VTs and suggests strongly (but does not prove) that the WCT is VT. (See “Implantable cardioverter-defibrillators: Overview of indications, components, and functions”.)

●Presence of a pacemaker – The patient should be asked about the presence of pacemaker, which raises the possibility of a device-associated WCT. (See ‘Supraventricular tachycardia’ below.)

●Atrial arrhythmias – In a patient known to have persistent atrial fibrillation (AF), a regular WCT is likely VT as aberrant conduction during AF would create an irregular rhythm. An exception is when AF “organizes” into atrial flutter; this can occur spontaneously but occurs much more commonly in the setting of antiarrhythmic drugs (especially class IC agents, amiodarone, or dronedarone).

●Age – In a patient over the age of 35 years, a WCT is likely to be VT (positive predictive value 85 percent in one series) [8]. SVT is more likely in younger patients (positive predictive value 70 percent). However, VT must be considered in younger patients, particularly those with a family history of ventricular arrhythmias or premature sudden cardiac death.

●Duration of the tachycardia – SVT is more likely if the tachycardia has recurred over a period of more than three years [5]. The first occurrence of the tachycardia after a myocardial infarction strongly implies VT [7].

●Symptoms – Symptoms are not useful in determining the diagnosis, but they are important as an indicator of the severity of hemodynamic compromise. Symptoms are primarily due to the elevated heart rate, associated heart disease, and the presence of left ventricular dysfunction [4,5,7]. Some patients with a WCT have few or no symptoms (palpitations, lightheadedness, diaphoresis), while others have severe manifestations including chest pain or angina, syncope, shock, seizures, and cardiac arrest [5].

Medications — Many medications have proarrhythmic effects, either directly by prolonging the QT interval or indirectly via alterations in electrolyte levels, and obtaining a medication history is among the first priorities in the evaluation of a patient with a WCT. The most common drug-induced WCT is a form of polymorphic VT called torsades de pointes (TdP). This arrhythmia is associated with QT interval prolongation when the patient is in sinus rhythm. Many medications (eg, antiarrhythmic drugs, anti-infective drugs, psychotropic drugs, etc) are known to prolong the QT interval (table 1) and are associated with a risk of polymorphic VT. An internet resource with updated lists of specific drugs that cause TdP is available at www.crediblemeds.org/. (See “Acquired long QT syndrome”, section on ‘Drug-induced TdP’.)

The class I antiarrhythmic drugs (table 2) can cause both aberrancy during an SVT and also VT. These drugs, especially class IC agents, slow conduction and have a property of “use-dependency” (a progressive decrease in impulse conduction velocity and wider QRS complex duration at faster heart rates). As a result, these drugs can cause rate-related aberration and a wide QRS complex during any SVT. However, they can also cause VT with a very wide, bizarre QRS, which may be incessant [9,10]. (See ‘Supraventricular tachycardia’ below and “Myocardial action potential and action of antiarrhythmic drugs”.)

Physical examination — As with the history, the initial physical examination should focus upon evidence of underlying cardiovascular disease which can impact the likelihood that the WCT is VT.

Findings suggestive of cardiovascular disease include:

●Signs of acute or chronic heart failure. (See “Treatment of acute decompensated heart failure: General considerations” and “Evaluation of the patient with suspected heart failure”.)

●A healed sternal incision as evidence of previous cardiothoracic surgery.

●The sequelae of peripheral artery disease or stroke.

●A pacemaker or ICD. These devices are usually palpable and are in the left or, less commonly, right pectoral area below the clavicle; some earlier ICDs are found in the anterior abdominal wall.

Ancillary testing — A number of additional tests may provide further insight to the mechanism of the tachycardia and the presence of associated conditions.

●Laboratory testing – Initial laboratory testing in all patients with a WCT should include electrolytes and cardiac troponin, with additional testing for elevated serum drug levels in patients taking certain medications.

•The plasma potassium and magnesium concentrations should be measured as part of the initial evaluation, since hypokalemia and hypomagnesemia both predispose to the development of VTs. Hyperkalemia can cause a wide QRS complex rhythm with the loss of a detectable P wave, although this usually is a supraventricular rhythm with a slow rate (so-called “sinoventricular rhythm”). (See “Causes and evaluation of hyperkalemia in adults” and “ECG tutorial: Miscellaneous diagnoses”, section on ‘Hyperkalemia’.)

•Cardiac troponin testing should be performed in patients with WCT, especially if the patient is having ongoing chest pain or hemodynamic instability. Cardiac troponin can be elevated in the setting of myocardial ischemia (as the result of myocardial oxygen supply and demand mismatch) or myocardial infarction (as a possible cause of the arrhythmia). Elevated cardiac troponin is associated with an increased risk of adverse outcomes and may guide hospital admission decisions, cardiac testing, and/or anti-ischemic therapy.

•In patients taking digoxin, quinidine, or procainamide, plasma concentrations of these drugs should be measured to assist in evaluating possible toxicity.

●Chest radiograph – A chest radiograph can provide evidence suggestive of structural heart disease, such as cardiomegaly. Evidence of previous cardiothoracic surgery and the presence of a pacemaker or ICD can also be detected.

Early diagnostic/therapeutic interventions — In patients with a WCT who are hemodynamically stable, certain vagal maneuvers (ie, carotid sinus massage) or the administration of certain intravenous medications (eg, adenosine, beta blockers, verapamil) may be both helpful for establishing the diagnosis and potentially therapeutic, although they do carry a risk of hemodynamic deterioration and should only be performed in closely monitored settings by experienced clinicians. These potential interventions are discussed in detail separately. (See “Approach to the management of wide QRS complex tachycardias”, section on ‘Vagal maneuvers’.)

EPIDEMIOLOGY — Ventricular tachycardia (VT) is the most common cause of wide complex tachycardia (WCT), particularly in patients with a history of cardiac disease. In series of unselected patients, VT accounted for up to 80 percent of cases of WCT [2,4,5,11]. VT frequency can exceed 90 percent in patients with structural heart disease (eg, those with a prior myocardial infarction) [7].

Supraventricular tachycardia (SVT) results in WCT much less frequently than VT. Among patients with WCT due to SVT, aberrant conduction is the most common reason for a widened QRS (21 percent of cases in one series) [11]. However, an aberrantly conducted SVT is still much less common than VT as the cause of WCT.

Antidromic atrioventricular reentrant tachycardia (AVRT) is a relatively uncommon cause of WCT (6 percent of cases in one series) [11].

CLINICAL MANIFESTATIONS — Patients with wide complex tachycardia (WCT) are rarely asymptomatic, although the type and intensity of symptoms will vary depending upon the rate of the WCT, the presence or absence of significant comorbid conditions, and whether the WCT is ventricular tachycardia (VT) or supraventricular tachycardia (SVT). Patients with WCT typically present with one or more of the following symptoms:

●Palpitations

●Chest pain

●Shortness of breath

●Syncope or presyncope

●Sudden cardiac arrest

Few physical examination findings in patients with a WCT are unique to WCT. By definition, patients will have a pulse exceeding 100 beats per minute related to the tachycardia. Patients may be hypotensive, which may result in alterations in consciousness. Patients with underlying heart disease in whom heart failure results from the WCT may have crackles on lung examination.

In addition, the physical examination in patients with WCT can reveal evidence of atrioventricular (AV) dissociation, which is present in up to 75 percent of patients with VT, although it is not always easy to detect [5,7,12]. During AV dissociation, the normal coordination of atrial and ventricular contraction is lost, which may produce characteristic physical findings. The presence of AV dissociation strongly suggests VT, although its absence is less helpful.

Although AV dissociation is typically diagnosed on the electrocardiogram (ECG), characteristic physical examination findings include (see ‘AV dissociation’below):

●Marked fluctuations in the blood pressure because of the variability in the degree of left atrial contribution to left ventricular filling, stroke volume, and cardiac output.

●Variability in the occurrence and intensity of heart sounds (especially S1) (“cacophony of heart sounds”), which is heard more frequently when the rate of the tachycardia is slower.

●Cannon “A” waves – Cannon A waves are intermittent and irregular jugular venous pulsations of greater amplitude than normal waves. They reflect simultaneous atrial and ventricular activation, resulting in contraction of the right atrium against a closed tricuspid valve. Prominent A waves can also be seen during some SVTs. Such prominent waves result from simultaneous atrial and ventricular contraction occurring with every beat. (See “Examination of the jugular venous pulse”.)

CAUSES OF WCT — Wide complex tachycardias (WCTs) most often result from ventricular tachycardia (VT), with other less common causes which include supraventricular tachycardia (SVT) with aberrant conduction, SVT with preexcitation, SVT with ventricular pacing, and some types of artifact mimicking WCT (table 3).

Ventricular tachycardia — VT usually originates within the ventricular myocardium, outside of the normal conduction system, resulting in direct myocardial activation. Compared with a normally conducted supraventricular beat (which activates the ventricular myocardium via the normal atrioventricular [AV] node-His-Purkinje system), ventricular activation during VT is slower and proceeds in a different sequence. Thus, the QRS complex is wide and abnormal (waveform 1). As there may be slight changes of the activation sequence during the VT, reflecting the abnormal pathway of impulse conduction, there may be subtle changes in QRS complex morphology or in the ST-T waves.

VT may be either monomorphic (having a uniform and a fairly stable QRS morphology during an episode), polymorphic (having a continuously varying QRS complex morphology and/or axis during an episode), or bidirectional (in which every other beat has a different axis as it travels alternately down different conduction pathways). The features of each form of VT are discussed separately. (See “Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation”and “Catecholaminergic polymorphic ventricular tachycardia and other polymorphic ventricular tachycardias with a normal QT interval” and “Congenital long QT syndrome: Epidemiology and clinical manifestations”.)

Artifact mimicking VT — ECG artifact, particularly when observed on a single-lead rhythm strip, may be misdiagnosed as VT (waveform 2) [13]. The presence of narrow-complex beats that can be seen to “march” through the supposed WCT at a fixed rate strongly supports the diagnosis of artifact.

Supraventricular tachycardia — When an SVT conducts to the ventricles via the normal AV node and His-Purkinje system, the activation wavefront spreads quickly through the ventricles and the QRS is usually narrow. In addition, the pathway of conduction to the ventricles is fixed and the same for each impulse, accounting for the uniformity of the QRS complexes and ST-T waves. However, SVT can also produce a widened QRS by a number of mechanisms, including aberrant conduction, preexcitation, and the activation of ventricular pacing.

Aberrant conduction — The conduction of a supraventricular impulse can be delayed or blocked in the bundle branches or in the distal Purkinje system, resulting in a wide, abnormal QRS. This phenomenon is referred to as aberrancy. (See “Basic approach to delayed intraventricular conduction”.)

Aberrant conduction may either be present at baseline or under certain conditions, such as faster heart rates.

●In patients with a left bundle branch block (LBBB), right bundle branch block (RBBB), or a nonspecific intraventricular conduction delay (IVCD) on their baseline electrocardiogram (ECG), any SVT will have a widened QRS. Thus, if time allows, review of a baseline ECG can be helpful in differentiating VT from SVT with aberrancy. The presence of a conduction abnormality on the baseline ECG does not prove that the tachycardia is SVT with aberrancy, but the more similar the QRS during the WCT is to the QRS during sinus rhythm, the more likely it is that the WCT is an SVT with aberrancy.

In patients with aberrancy at baseline who manifest a WCT in which the QRS complex is narrower than the baseline QRS, the WCT is likely VT originating near the ventricular septum, with early engagement of the specialized conducting system. This scenario is extremely unusual.

●In patients with a narrow QRS complex at baseline which widens at faster heart rates, conduction is normal during sinus rhythm but aberrant during the tachycardia. The most common reason for this is rate-related aberration (functional bundle branch block), in which rapidly generated impulses reach the conducting fibers before they have fully recovered from the previous impulse. Such a delay in recovery may also be the result of underlying disease of the His-Purkinje system, hyperkalemia, or the actions of antiarrhythmic drugs, particularly the class IC agents (eg, flecainide, propafenone). (See “Myocardial action potential and action of antiarrhythmic drugs”.)

Preexcitation syndrome — In the preexcitation syndromes, AV conduction can occur over the normal conduction system and also via an accessory AV pathway (figure 1A-C). These two pathways create the anatomic substrate for a reentrant circuit (macroreentrant circuit), facilitating the development of a circus movement or reentrant tachycardia known as atrioventricular reentrant tachycardia (AVRT). (See “ECG tutorial: Preexcitation syndromes” and “Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway”, section on ‘Orthodromic AVRT’ and “Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway”, section on ‘Antidromic AVRT’.)

AVRT can present with a narrow or a wide QRS complex:

●If antegrade conduction to the ventricles occurs over the AV node and retrograde conduction is over the accessory pathway, the QRS complex will be narrow (unless there is aberrant conduction at baseline with a wide QRS complex). This narrow complex AVRT is known as an orthodromic AVRT (figure 2 and waveform 3). Orthodromic AVRT can also occur with rate-related aberrancy, creating a WCT.

●If antegrade conduction occurs over an accessory pathway and retrograde conduction occurs over the AV node or a second accessory pathway, the QRS complex will be wide with an unusual morphology. This is known as an antidromic AVRT (figure 3 and waveform 4). Antidromic AVRT is difficult to differentiate from VT, because ventricular activation starts outside the normal intraventricular conduction system in both types of tachycardia (ie there is direct myocardial activation). (See ‘VT versus AVRT’below.)

In addition, patients with an accessory pathway may develop a different SVT (eg, atrial tachycardia, atrial fibrillation [AF], or atrial flutter). In such cases, the atrial impulses may use the accessory pathway to conduct to the ventricles, and the QRS could be either narrow or wide, depending upon whether ventricular activation occurs over the normal conduction system, the accessory pathway, or both (waveform 5 and waveform 6 and waveform 7). (See “Epidemiology, clinical manifestations, and diagnosis of the Wolff-Parkinson-White syndrome”, section on ‘Arrhythmias associated with WPW’.)

Pacemakers — When the ventricles are activated by a pacing device, the QRS complex is generally wide:

●Most transvenous ventricular pacemakers pace the right ventricle, causing a wide QRS complex of the LBBB type. Typically, the surface ECG shows a broad R wave in lead I, indicating conduction from right to left. (See “Overview of cardiac pacing in heart failure”.)

●Pacemakers used in cardiac resynchronization therapy (CRT) usually pace both ventricles. Although CRT generates a QRS complex that is narrower than the patient’s baseline (a chronically widened QRS is one of the components of the indication for CRT), it is still usually longer than 120 msec. The surface ECG typically shows a Q wave or QS complex in lead I, indicating activation from left to right. (See “Cardiac resynchronization therapy in heart failure: Indications”.)

Recognizing that a QRS complex is due to ventricular pacing can be challenging, particularly during a tachycardia. In addition to characteristic QRS morphology, a pacing “spike” or stimulus artifact can often be identified. The stimulus artifact is a narrow electrical signal too rapid to represent myocardial depolarization.

Among patients with a pacemaker or an ICD, further possibilities need to be considered in addition to the usual differential diagnosis of a WCT. These include:

●In the presence of sinus tachycardia or some SVTs (eg, an atrial tachycardia, AF, or atrial fibrillation), the device may “track” the atrial impulse and pace the ventricle at the rapid rate, resulting in a WCT. (See “Modes of cardiac pacing: Nomenclature and selection”, section on ‘Mode switching’.)

●A WCT can result if ventricular paced beats are conducted retrograde (backward) through the AV node to the atrium, resulting in an atrial signal, which the pacemaker senses and tracks with another ventricular stimulus. This ventricular paced beat is also conducted retrograde, and the cycle repeats indefinitely, a process termed pacemaker-mediated tachycardia (PMT) or endless loop tachycardia. PMT usually occurs at the upper rate limit. A different mechanism of pacemaker-associated tachycardia, non-reentrant repetitive VA synchrony, also creates a wide complex rhythm, but usually at the lower rate limit or sensor mediated rate rather than at the upper rate limit.

These and other arrhythmias associated with pacemakers are discussed in detail separately. (See “Unexpected rhythms with normally functioning dual-chamber pacing systems”, section on ‘Pacemaker-mediated tachycardia’.)

EVALUATION OF THE ELECTROCARDIOGRAM — In most patients, a probable diagnosis (ventricular tachycardia [VT] or supraventricular tachycardia [SVT]) may be made by closely reviewing the electrocardiogram (ECG), although definitive diagnosis is not always possible and may be time-consuming, especially for clinicians unfamiliar with the criteria for distinguishing VT from SVT. To perform an adequate ECG analysis, both a 12-lead ECG and a rhythm strip should be obtained. If available, a previous ECG when the patient was in normal sinus rhythm may be helpful. However, if there are any questions regarding the patient’s stability, detailed ECG evaluation should be deferred in favor of urgent therapy, although if time allows, an ECG should be obtained for later review prior to urgent cardioversion. (See “Approach to the management of wide QRS complex tachycardias”, section on ‘Unstable patients’.)

Basic features — As with the interpretation of any ECG, the standard initial approach includes an assessment of rate, regularity, axis, QRS duration, and QRS morphology.

●Rate – The rate of the wide complex tachycardia (WCT) is of limited use in distinguishing VT from SVT. When the rate is approximately 150 beats per minute, atrial flutter with 2:1 atrioventricular (AV) block and with aberrant conduction should be considered, although this diagnosis should not be accepted without other supporting evidence.

●Regularity – VT is generally regular, although slight variation in the RR intervals is sometimes seen. Slight irregularity suggests VT as opposed to most SVTs, which are characterized by uniformity of the RR intervals. When the onset of the arrhythmia is available for analysis, a period of irregularity (“warm-up phenomenon”), suggests VT. More marked irregularity of RR intervals occurs in polymorphic VT and in atrial fibrillation (AF) with aberrant conduction.

●Morphology – When describing WCTs, the QRS morphology in lead V1 is the key. If the complex is primarily negative in lead V1, the WCT is said to be left bundle branch block (LBBB)-like. If the QRS is primarily positive in lead V1, the WCT is said to be right bundle branch block (RBBB)-like. (See ‘QRS morphology’ below.)

●Axis – The QRS axis in the frontal plane can be useful in distinguishing SVT from VT. (See “Basic principles of electrocardiographic interpretation”, section on ‘QRS axis’.)

•A right superior axis (axis from -90 to ±180 degrees), sometimes called an indeterminate or “northwest” axis, is rare in SVT and strongly suggests VT [5]. There are two exceptions to this rule. The first is an antidromic atrioventricular reentrant tachycardia (AVRT) seen with ventricular preexcitation. In this situation there is direct activation of the ventricular myocardium, bypassing the normal His-Purkinje system, and the QRS complex may have an indeterminate axis. The second is a biventricular pacemaker in which the axis is often indeterminate with an initial Q wave in lead I.

•Compared with the axis during sinus rhythm (when an old ECG is available for review), an axis shift during the WCT of more than 40 degrees suggests VT [14].

•In a patient with a RBBB-like WCT, a QRS axis to the left of -30 degrees suggests VT. (See ‘QRS morphology’ below.)

•In a patient with an LBBB-like WCT, a QRS axis to the right of +90 degrees suggests VT [15]. (See ‘QRS morphology’ below.)

●QRS duration – In general, a wider QRS favors VT. In a RBBB-like WCT, a QRS duration >140 msec suggests VT; while in a LBBB-like WCT, a QRS duration >160 msec suggests VT [5,15]. (See ‘QRS morphology’ below.)

In an analysis of several studies, a QRS duration >160 msec was a strong predictor of VT (likelihood ratio >20:1) [16]. However, a QRS duration >160 msec is not helpful in some settings, including SVT with an AV accessory pathway; the presence of drugs capable of slowing intraventricular conduction, such as class I antiarrhythmic drugs; and in association with hyperkalemia [15,17,18]. A very wide QRS complex may also be seen with a dilated cardiomyopathy in which diffuse fibrosis may produce a marked slowing of impulse conduction through the ventricular myocardium. (See ‘VT versus AVRT’ below and ‘Medications’above.)

A QRS duration <140 msec does not exclude VT, since VT originating from the septum or within the His-Purkinje system (as opposed to the myocardium) may be associated with a relatively narrow QRS complex. (See “Monomorphic ventricular tachycardia in the absence of apparent structural heart disease”, section on ‘Idiopathic left ventricular tachycardia’.)

Concordance — Concordance is present when the QRS complexes in all six precordial leads (V1 through V6) are monophasic with the same polarity. They can either all be entirely positive with tall, monophasic R waves, or all be entirely negative with deep monophasic QS complexes. If any of the six leads has a biphasic QRS (qR or RS complexes), concordance is not present.

●Negative concordance is strongly suggestive of VT but is not definitive. Rarely, SVT with LBBB aberrancy will demonstrate negative concordance, but there is almost always some evidence of an R wave in the lateral precordial leads.

●Positive concordance is most often due to VT but can also occur in the relatively rare case of antidromic AVRT with a left posterior accessory pathway [5,15]. (See “Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome”.)

While the presence of concordance strongly suggests VT (>90 percent specificity), its absence is not helpful diagnostically (approximately 20 percent sensitivity) [11].

AV dissociation — AV dissociation is characterized by atrial activity that is independent of ventricular activity (waveform 8).

In a WCT with AV dissociation, an atrial rate slower than the ventricular rate strongly suggests VT. An atrial rate that is faster than the ventricular rate is seen with some SVTs, such as atrial flutter or an atrial tachycardia with 2:1 AV conduction. In these settings, however, there is a consistent relationship between the P waves and the QRS complexes, so there is not true AV dissociation.

While the presence of AV dissociation largely establishes VT as the diagnosis, its absence is not as helpful for two reasons:

●AV dissociation may be present but not obvious on the ECG.

●In some cases of VT, the ventricular impulses conduct backwards through the AV node and capture the atrium (referred to as 1:1 retrograde conduction), so in fact there is AV association rather than AV dissociation [19]. This may be seen more commonly when the rate of VT is slower. VT with retrograde Wenckebach conduction, or with 2:1 VA conduction, technically does not exhibit AV dissociation, though the ventricular rate exceeds the atrial rate. In all cases in which there is retrograde VA conduction, the P waves will be inverted in the inferior leads.

Dissociated P waves — P waves are said to be dissociated if they are not consistently coupled to the QRS complexes, as evidenced by the following:

●PP and RR intervals are different

●PR intervals are variable

●There is no association between P and QRS complexes

●The presence of a P wave with one, but not all, QRS complexes

During a WCT, P waves are often difficult to identify. If P waves are not evident on the surface ECG, direct recordings of atrial activity (eg, via an implanted pacemaker or implantable cardioverter-defibrillator [ICD], or via an esophageal electrode or temporary pacing catheter or epicardial pacing wires after heart surgery) can reveal AV dissociation [20].

Fusion and capture beats — Fusion and/orcapture beats, when identified on the surface ECG in a patient with WCT, are diagnostic for VT.

●Fusion beats occur when one impulse originating from the ventricle and a second supraventricular impulse simultaneously activate the ventricular myocardium. The resulting QRS complex has a morphology intermediate between that of a sinus beat and a purely ventricular complex (waveform 9). Intermittent fusion beats during a WCT are diagnostic of AV dissociation and therefore of VT.

●Capture beats, or Dressler beats, are QRS complexes during a WCT that are identical to the sinus QRS complex (waveform 9). The term “capture beat” implies that the normal conduction system has momentarily “captured” control of ventricular activation from the VT focus.

Fusion beats and capture beats are more commonly seen when the tachycardia rate is slower.

QRS morphology — Frequently, the above criteria do not provide a definitive diagnosis. Further ECG evaluation involves assessment of the morphology of the QRS complex.

Analysis of QRS morphology is based upon an understanding of the relationships between the sites of tachycardia origin, ventricular activation patterns, and the resulting morphologies of the QRS complex in the 12 standard ECG leads.

Diagnostic criteria — A number of criteria have been developed to facilitate the evaluation of QRS morphology. Most of these approaches involve classifying the WCTs as having one of two patterns:

●An RBBB-like pattern – QRS polarity is positive in lead V1

●An LBBB-like pattern – QRS polarity is negative in lead V1

This distinction does not, by itself, make the diagnosis, but additional features favor VT in either RBBB-like or LBBB-like WCTs. However, the value of these morphologic criteria is subject to several limitations:

●Associations between the QRS morphology and WCT diagnosis are often based upon statistical correlations with substantial overlap.

●Morphologic criteria favoring VT can be present in patients with an intraventricular conduction delay or bundle branch block during sinus rhythm, limiting their applicability in these cases [21]. On occasion a rate-related bundle branch block may have atypical features, suggesting VT.

●Morphologic criteria tend to misclassify antidromic AVRT as VT. They may also misclassify SVT associated with a cardiomyopathy. (See ‘VT versus AVRT’ below.)

In the discussions that follow, upper- and lower-case letters are used to indicate the relative magnitude of the described electrocardiographic waves. As examples, the term “qR” implies a small Q wave followed by a large R wave.

●V1-positive (RBBB) pattern – In the patient with a WCT and positive QRS polarity in lead V1, the following associations have been made [5,11,15,22-24]:

•Findings in lead V1 – A monophasic R or biphasic qR complex in lead V1 favors VT.

A triphasic RSR’ or RsR’ complex (the so-called “rabbit-ear” sign) in lead V1 usually favors SVT. As an exception, if the left peak of the RsR’ complex is taller than the right peak, VT is more likely [16,25].

•Findings in lead V6 – An rS complex (R wave smaller than S wave) in lead V6 favors VT [16]. By contrast, an Rs complex (R wave larger than S wave) in lead V6 favors SVT.

●V1-negative (LBBB) pattern – In the patient with a WCT and negative QRS polarity in lead V1, the following associations have been made [5,11,15,22-24]:

•Findings in lead V1 or V2 – A broad initial R wave of 40 msec duration or longer in lead V1 or V2 favors VT. In contrast, the absence of an initial R wave or a small initial R wave of less than 40 msec in lead V1 or V2 favors SVT.

Two other findings that favor VT are a slurred or notched downstroke of the S wave in lead V1 or V2, and a duration from the onset of the QRS complex to the nadir of the QS or S wave of ≥60 msec in lead V1 or V2. In an analysis of several studies, the presence of any of these three criteria (broad R wave, slurred or notched downstroke of S wave, and delayed nadir of S wave) was a strong predictor of VT [16].

By contrast, a swift, smooth downstroke of the S wave in lead V1 or V2 with a duration of <60 msec favors SVT.

•Findings in lead V6 – The presence of any Q or QS wave in lead V6 favors VT [16]. By contrast, the absence of a Q wave in lead V6 favors SVT.

Variation in QRS and ST-T shape — Subtle, non-rate-related fluctuations or variations in QRS and ST-T wave configuration suggest VT and may reflect variations in the VT reentrant circuit within the myocardium as well as a subtle difference in the activation sequence of the myocardium reflecting activation that bypasses the normal conduction system. AV dissociation can cause variability in the ST segment and T wave morphology. By contrast, SVT, because it follows a fixed conduction pathway to and through the ventricular myocardium, is characterized by uniformity of QRS and ST-T shape unless the rate changes.

DIAGNOSIS — Most patients with wide complex tachycardia (WCT) will have some, but not all, of the electrocardiogram (ECG) features favoring ventricular tachycardia (VT). There is no single criterion or combination of criteria that provides complete diagnostic accuracy in evaluating a WCT. It is typically necessary, therefore, to integrate multiple ECG findings into a diagnostic strategy. Several strategies have been proposed, of which the Brugada criteria are the most widely known [16,26,27]. (See ‘Brugada criteria’ below.)

However, because the diagnosis of a WCT cannot always be made with complete certainty even when using multiple ECG criteria, an unknown or uncertain rhythm should be presumed to be VT in the absence of contrary evidence [28]. VT is far more common than supraventricular tachycardia (SVT), by a factor of four in unselected populations and by as much as 10-fold in patients with prior myocardial infarction. Additionally, presuming VT guards against inappropriate and potentially dangerous therapies directed at an SVT which can precipitate hemodynamic deterioration in patients with VT, and treatment of SVT as if it were VT is safe and frequently effective in restoring sinus rhythm. (See “Approach to the management of wide QRS complex tachycardias”, section on ‘Management’.)

An algorithmic approach to the diagnosis of a WCT will be reviewed here, with emphasis on the distinction between VT and SVT. The approach to a narrow QRS complex tachycardia is discussed separately. (See “Clinical manifestations, diagnosis, and evaluation of narrow QRS complex tachycardias”.)

Our approach — Once a WCT has been identified on the ECG, prompt diagnosis and management is important. Unstable patients should be presumed to have VT and treated as such. While the Brugada criteria are the most widely known and applied criteria for distinguishing VT from SVT, time and/ortechnical limitations may not allow for immediate review of the ECG in such detail, particularly in a symptomatic or borderline unstable patient. Our approach emphasizes immediate ECG review for key high-yield features in parallel with a brief history that can guide the management of most patients with a WCT.

●Is the rhythm regular or irregular? – VT and most SVTs are generally regular, though slight variation of the RR interval can be seen in VT. An irregular WCT usually represents atrial fibrillation (AF) with aberrant conduction, although polymorphic VT should also be considered. (See ‘Basic features’ above.)

●What is the QRS axis? – A right superior axis (axis from -90 to ±180 degrees) strongly favors VT, as does any axis shift of greater than 40 degrees when compared with baseline or concordance of the QRS complexes. (See ‘Basic features’ above and ‘Concordance’above.)

●Is there atrioventricular (AV) dissociation? – If AV dissociation can be quickly identified, an atrial rate slower than the ventricular rate, along with any fusion or capture beats, strongly suggests VT. (See ‘AV dissociation’ above.)

●Is there a history of heart disease or arrhythmias? – A quick history focusing on structural heart disease, particularly coronary heart disease and/or prior myocardial infarction, as well as any known arrhythmias or cardiac implantable electronic devices (eg, pacemaker or implantable cardioverter-defibrillator [ICD]), can aid in identifying the most likely etiology of WCT. The WCT is far more likely to be VT in patients over 35 years of age with known coronary heart disease or prior myocardial infarction, and in those with an ICD. (See ‘History’ above.)

The absence of the historical or ECG features of VT does not confirm a diagnosis of SVT. The diagnosis of SVT should be considered primarily in young patients, whose hearts are structurally normal, 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. When the diagnosis of a WCT remains uncertain, we recommend that the patient be treated as if the rhythm is VT until definitively proven otherwise.

Brugada criteria — The Brugada criteria are a stepwise approach in which four criteria for VT are sequentially assessed (algorithm 1) [26]. If any of the criteria is satisfied, the diagnosis of VT is made, and if none are fulfilled, an SVT is diagnosed. An exception is an antidromic atrioventricular reentrant tachycardia (AVRT) in Wolff-Parkinson-White syndrome.

The steps are as follows:

●Leads V1-V6 are inspected to detect an RS complex. If there are no RS complexes, concordance is present and the diagnosis of VT can be made. (See ‘Concordance’ above.)

●If an RS complex is present, measure the interval between the onset of the R wave and the nadir of the S wave (RS interval). If the longest RS interval in any lead is >100 msec and the R wave is wider than the S wave, the diagnosis of VT can be made. This reflects that with VT, the entire QRS complex is wide and abnormal (even the initial R wave portion), while aberration is due to a terminal delay resulting in a wider terminal portion of the QRS complex (ie, S wave).

This criterion, however, may be limited in the presence of an underlying diffuse cardiomyopathy, as in this situation even initial ventricular activation may be slow and abnormal.

●If the longest RS interval is <100 msec, the presence or absence of AV dissociation is assessed. If AV dissociation is seen, the diagnosis of VT is made. (See ‘AV dissociation’above.)

●If AV dissociation cannot clearly be demonstrated, the QRS morphology criteria for V1-positive and V1-negative wide QRS complex tachycardias are considered. QRS morphology criteria consistent with VT must be present in leads V1 or V2 and in lead V6 to diagnose VT. If either the V1-V2 or the V6 criteria are not consistent with VT, an SVT is assumed. (See ‘QRS morphology’ above.)

Alternative approaches — Several alternative approaches have been proposed in the literature, although none are as commonly used as the Brugada criteria. These approaches are generally best performed in consultation with an electrophysiologist with expertise in the diagnosis of WCT.

●An alternative algorithm (Vereckei approach) uses a stepwise approach similar to the Brugada criteria, but includes different ECG features (algorithm 2) [27]. Two unique features of this algorithm include an initial R wave in aVR (diagnostic of VT), and the Vi:Vt ratio. Vi and Vt are the magnitude of voltage change in the initial and terminal 40 msec of a QRS, respectively. Vi and Vt should be measured from the same biphasic or multiphasic QRS complex. A Vi:Vt ratio ≤1 is diagnostic of VT.

One study of 51 patients with WCT induced during electrophysiology study showed equivalent sensitivity for diagnosis between the Vereckei and Brugada approaches (89 versus 90 percent), but the Vereckei approach yielded significantly fewer incorrect diagnoses following the first step (2 versus 27 percent) and was slightly faster to perform (9.1 versus 9.9 seconds) [29].

●A Bayesian approach utilizes likelihood ratios (LR) for six ECG criteria [16]. Patients are presumed to start with a “prior odds ratio” of 4.0 (4:1) in favor of VT. As each criterion is evaluated sequentially, the associated LR is multiplied by the prior odds ratio to calculate the new probability of VT. The final odds ratio (posterior probability) is considered consistent with VT if the value is ≥1.0, and SVT if the value is <1.0.

●Intravenous adenosine may be administered as both a diagnostic and potentially therapeutic agent. (See “Approach to the management of wide QRS complex tachycardias”, section on ‘Pharmacologic interventions’.)

VT versus AVRT — Differentiation between VT and antidromic AVRT is particularly difficult. Because there is direct myocardial activation since ventricular activation begins outside of the normal conduction system in both VT and antidromic AVRT, many of the standard criteria are not able to discriminate antidromic AVRT from VT. The clinical significance of this problem is often limited, however, because preexcitation is an uncommon cause of WCT (6 percent in one series), particularly if other clinical factors (eg, age, underlying heart disease) suggest VT [11].

For cases in which preexcitation is thought to be likely (such as a young patient without structural heart disease, or a patient with a known accessory pathway), a separate algorithm was developed which consists of the following three steps (algorithm 3) [26]:

●The predominant polarity of the QRS complex in leads V4 through V6 is defined either as positive or negative. If predominantly negative, the diagnosis of VT can be made.

●If the polarity of the QRS complex is predominantly positive in V4 through V6, the ECG should be examined for the presence of a qR complex in one or more of precordial leads V2 through V6. If a qR complex can be identified, VT can be diagnosed.

●If a qR wave in leads V2 through V6 is absent, the AV relationship is then evaluated (AV dissociation). If a 1:1 AV relationship is not present and there are more QRS complexes present than P waves, VT can be diagnosed.

When any of these criteria are met, VT is likely. However, if the ECG does not display any of the three morphologic characteristics diagnostic of VT in this algorithm, the diagnosis of antidromic AVRT must be considered. Importantly, the QRS complex morphology and ST-T waves are uniform with AVRT as every impulse to the ventricle is conducted through the same accessory pathway.

Algorithm performance — Algorithms often perform well in initial reports. However, such studies include selected populations and experienced ECG analysts.

●In its initial description, the reported sensitivity and specificity of the Brugada criteria were 98.7 and 96.5 percent, respectively [26]. However, in two subsequent reports in which a total of nine clinicians (two cardiologists, two emergency department clinicians, and five internists) used these criteria in interpreting a total of 168 WCTs that had been diagnosed with electrophysiologic testing, the sensitivity ranged from 79 to 92 percent, and specificity from 43 to 70 percent [30,31].

●In a comparison of the Brugada criteria and the Bayesian approach, the two approaches performed similarly, with sensitivities of 92 and 97 and specificities of 44 and 56 percent, respectively [31].

●In the initial description of the alternative algorithm described above, it was significantly more accurate than the Brugada criteria [27]. Further study is necessary to confirm both the overall accuracy of this approach and its superiority to the Brugada criteria.

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”.)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^thto 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

●Basics topics (see “Patient education: Ventricular tachycardia (The Basics)”)

SUMMARY AND RECOMMENDATIONS

●Ventricular tachycardia (VT) is the most common cause of wide complex tachycardia (WCT), particularly in patients with a history of cardiac disease, while supraventricular tachycardia (SVT) results in WCT (due to aberrant conduction, preexcitation, or ventricular pacing) much less frequently. WCT is identified as VT in up to 80 percent of unselected patients and more than 90 percent of patients with known structural heart disease. (See ‘Epidemiology’ above and ‘Causes of WCT’above.)

●Patients with WCT are rarely asymptomatic, although the type and intensity of symptoms will vary depending upon the rate of the WCT, the presence or absence of significant comorbid conditions, and whether the WCT is VT or SVT. Patients with WCT typically present with one or more of palpitations, chest pain, shortness of breath, syncope/presyncope, or sudden cardiac arrest. (See ‘Clinical manifestations’ above.)

●The first priority when evaluating a patient with a WCT is an immediate assessment of patient stability, including the patient’s symptoms, vital signs, and the level of consciousness. An unstable patient will have evidence of hemodynamic compromise, such as hypotension, altered mental status, chest pain, or heart failure.

•A patient who is unresponsive or pulseless should be treated according to standard advanced cardiac life support (ACLS) algorithms (algorithm 4). (See ‘Assessment of stability’ above and “Advanced cardiac life support (ACLS) in adults”.)

•For a patient who is unstable but conscious, we recommend immediate synchronized cardioversion (Grade 1B). (See ‘Assessment of stability’ above and “Approach to the management of wide QRS complex tachycardias”, section on ‘Unstable patients’.)

•In a stable patient, or following cardioversion to stabilize an unstable patient, our initial approach includes the following:

-A succinct history and physical examination, focusing on the presence of structural heart disease, especially coronary heart disease and/or a previous myocardial infarction, as well as the history of any arrhythmias and the presence of a pacemaker or implantable cardioverter defibrillator (ICD). (See ‘History’ above and ‘Physical examination’ above.)

-Review of the patient’s medications for drugs which may be proarrhythmic (by prolonging the QT interval or promoting electrolyte disturbances). (See ‘Medications’ above.)

-Ancillary testing including serum electrolyte levels, cardiac troponin, and a chest radiograph in all patients. (See ‘Ancillary testing’ above.)

●In most patients with WCT, a probable diagnosis (VT or SVT) may be made by closely reviewing the electrocardiogram (ECG), although definitive diagnosis is not always possible and may be time-consuming. The standard initial approach to ECG interpretation includes an assessment of rate, regularity, axis, QRS duration, and QRS morphology. (See ‘Evaluation of the electrocardiogram’ above.)

●Most patients with WCT will have some, but not all, of the ECG features favoring VT. There is no single criterion or combination of criteria that provides complete diagnostic accuracy in evaluating a WCT, even when employing an algorithmic approach to the diagnosis of a WCT, most commonly using the Brugada criteria. (See ‘Diagnosis’ above.)

•ECG features consistent with VT include concordance, AV dissociation, fusion/capture beats, and specific QRS morphologies.

•The absence of the historical or ECG features of VT does not confirm a diagnosis of SVT. The diagnosis of SVT should be considered primarily in young patients, whose hearts are structurally normal, 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.

•When the diagnosis of a WCT is uncertain, we recommend that the patient be treated as if the rhythm is VT (Grade 1B).

ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge Philip Podrid, MD, who contributed to an earlier version of this topic review.

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

Topic 920 Version 22.0

Approach to the diagnosis of wide QRS complex tachycardias

Bình luận

Để lại một bình luận Hủy

Thêm bài viết

UNG THƯ ĐẦU TỤY UNG THƯ QUANH BÓNG VATER – Nguyễn Cao Cương BV Bình Dân & ĐHYK Phạm Ngọc Thạch

QUY TRÌNH CHĂM SÓC BỆNH NHÂN CHẤN THƯƠNG THẬN

CHẨN ĐOÁN VÀ ĐIỀU TRỊ VIÊM PHỔI HOẠI TỬ Ở TRẺ EM

CHĂM SÓC BỆNH NHÂN TAI BIẾN MẠCH MÁU NÃO