Abstract
Wide complex tachycardia (WCT) is a rhythm with a rate of more than 100 beats/min and a QRS duration of more than 120 milliseconds. Several arrhythmias can manifest as WCTs; the most common is ventricular tachycardia (VT), which accounts for 80% of all cases of WCT. Supraventricular tachycardias (SVTs) with aberrancy account for 15% to 20% of WCTs. SVTs with bystander preexcitation and antidromic atrioventricular reentrant tachycardia account for 1% to 6% of WCTs.
Determination of the cause of the WCT (particularly distinguishing between VT and SVT) is necessary to guide subsequent management decisions. Accurate diagnosis of the WCT requires information obtained from the history, physical examination, response to certain maneuvers, and careful inspection of the ECG, including rhythm strips and 12-lead tracings. Comparison of the ECG during the tachycardia with that recorded during sinus rhythm, if available, can also provide valuable information.
Several algorithms integrating findings on the surface ECG (including QRS axis, duration, and morphology) have been proposed to help distinguish VT from aberrantly conducted SVT. Differentiation between VT and preexcited SVT, on the other hand, remains particularly difficult, because ventricular activation begins outside the normal intraventricular conduction system in both tachycardias. As a result, the algorithms for WCT and most of the traditional QRS morphology criteria tend to misclassify SVTs with preexcitation as VT.
Keywords
wide complex tachycardia, ventricular tachycardia, supraventricular tachycardia, aberrant conduction, ventricular preexcitation
Outline
Clinical Considerations, 730
Causes of Wide Complex Tachycardias, 730
Clinical History, 730
Physical Examination, 731
Laboratory Testing, 732
Pharmacological Intervention, 732
Electrocardiographic Features, 732
Ventricular Tachycardia Versus Aberrantly Conducted Supraventricular Tachycardia, 732
Algorithms for the Electrocardiographic Diagnosis of Wide Complex Tachycardia, 738
Ventricular Tachycardia Versus Preexcited Supraventricular Tachycardia, 742
Limitations of Electrocardiographic Criteria for Diagnosis of Wide Complex Tachycardia, 742
Electrophysiological Testing, 742
Baseline Observations During Normal Sinus Rhythm, 742
Induction of Tachycardia, 743
Tachycardia Features, 743
Diagnostic Maneuvers During Tachycardia, 744
Clinical Considerations
Causes of Wide Complex Tachycardias
A narrow QRS complex (120 milliseconds or less) requires rapid, highly synchronous electrical activation of the right ventricle (RV) and left ventricle (LV), which can only be achieved through the specialized, rapidly conducting His-Purkinje system (HPS). A wide QRS complex implies less synchronous ventricular activation of longer duration, which can be due to intraventricular conduction disturbances (IVCDs), or ventricular activation not mediated by the His bundle (HB) but by a bypass tract (BT) (preexcitation) or from a site within a ventricle (ventricular arrhythmias). IVCDs can be fixed and present at all heart rates, and they can be intermittent and related to either tachycardia or bradycardia. IVCDs can be caused by structural abnormalities in the HPS or ventricular myocardium or by functional refractoriness in a portion of the conduction system (i.e., aberrant ventricular conduction).
Wide complex tachycardia (WCT) is a rhythm with a rate of more than 100 beats/min and a QRS duration of more than 120 milliseconds ( Fig. 21.1 ). Several arrhythmias can manifest as WCTs ( Table 21.1 ); the most common is ventricular tachycardia (VT), which accounts for 80% of all cases of WCT. Supraventricular tachycardia (SVT) with aberrancy accounts for 15% to 20% of WCTs. SVTs with bystander preexcitation and atrioventricular reentrant tachycardia (AVRT) account for 1% to 6% of WCTs.
| Cause | Description, Examples |
|---|---|
| VT | Macroreentrant VT Focal VT |
| SVT with aberrancy | Functional BBB Preexistent BBB |
| Preexcited SVT | Antidromic AVRT AT or AVNRT with bystander BT |
| SVT with preexisting nonaberration QRS abnormality | Bizarre QRS patterns in repaired congenital heart disease, cardiac malpositions, unusual hypertrophy patterns |
| SVT with antiarrhythmic drugs | Class IA and IC agents |
| Electrolyte abnormalities | Hyperkalemia |
| Ventricular pacing | |
In the stable patient who will undergo a more detailed assessment, the goal of evaluation should include determination of the cause of the WCT (particularly distinguishing between VT and SVT). Accurate diagnosis of the WCT requires information obtained from the history, physical examination, response to certain maneuvers, and careful inspection of the electrocardiogram (ECG), including rhythm strips and 12-lead tracings. Comparison of the ECG during the tachycardia with that recorded during sinus rhythm, if available, can also provide valuable information.
Clinical History
Age
WCT in a patient older than 35 years is likely to be VT (positive predictive value of up to 85%). SVT is more likely in the younger patient (positive predictive value of 70%).
Symptoms
Some patients with WCT present with few or no symptoms (e.g., palpitations, lightheadedness, diaphoresis), whereas others can have severe manifestations, including chest pain, dyspnea, syncope, seizures, and cardiac arrest. The severity of symptoms during a WCT is not useful in determining the tachycardia mechanism because symptoms are primarily related to the fast heart rate, associated heart disease, and the presence and extent of LV dysfunction, rather than to the mechanism of the tachycardia. It is important to recognize that VT does not necessarily result in hemodynamic compromise or collapse; on the other hand, rapid SVT can cause decompensation in susceptible patients. Misdiagnosis of VT as SVT on the basis of hemodynamic stability is a common error that can lead to inappropriate and potentially dangerous therapy.
Duration of the Arrhythmia
SVT is more likely if the tachycardia has recurred over a period of more than 3 years. The first occurrence of a WCT after myocardial infarction (MI) strongly implies VT.
Presence of Underlying Heart Disease
The presence of structural heart disease, especially coronary heart disease and a previous MI, strongly suggests VT as the cause of WCT. In one report, more than 98% of patients with a previous MI had VT as the cause of WCT, whereas only 7% of those with SVT had an MI. It should be realized, however, that VT can occur in patients with no apparent heart disease, and SVT can occur in those with structural heart disease.
Pacemaker or Implantable Cardioverter-Defibrillator Implantation
A history of pacemaker or implantable cardioverter-defibrillator (ICD) implantation should raise the possibility of a device-associated tachycardia. Ventricular pacing can be associated with a small and almost imperceptible stimulus artifact on the ECG. The presence of an ICD is also of importance because such a device should identify and treat a sustained tachyarrhythmia, depending on device programming, and because the presence of an ICD implies that the patient is known to have an increased risk of ventricular tachyarrhythmias.
Medications
Many different medications have proarrhythmic effects. The most common drug-induced tachyarrhythmia is torsades de pointes. Frequently implicated agents include antiarrhythmic drugs (such as sotalol, dofetilide, and quinidine) and certain antimicrobial drugs (such as erythromycin). Diuretics are a common cause of hypokalemia and hypomagnesemia, which can predispose to ventricular tachyarrhythmias, particularly torsades de pointes in patients taking antiarrhythmic drugs. Furthermore, class I antiarrhythmic drugs, especially class IC agents, can decrease conduction velocity at faster heart rates (use dependency). As a result, these drugs can cause aberration and widening of the QRS complex during any tachyarrhythmia.
Digoxin can cause almost any cardiac arrhythmia, especially with increasing plasma digoxin concentrations above 2.0 ng/mL (2.6 mmol/L). Digoxin-induced arrhythmias are more frequent at any given plasma concentration if hypokalemia is also present. The most common digoxin-induced arrhythmias include monomorphic VT (often with a relatively narrow QRS complex), bidirectional VT (a regular alternation of two wide QRS morphologies, each with a different axis), and nonparoxysmal junctional tachycardia.
Physical Examination
Most of the elements of the physical examination, including the blood pressure and heart rate, are of importance primarily in determining the presence and severity of hemodynamic instability and, thus, how urgently a therapeutic intervention is required. In patients with significant hemodynamic compromise, a thorough diagnostic evaluation should be postponed until acute management has been addressed. In this setting, emergency cardioversion is the treatment of choice and does not require knowledge of the mechanism of the arrhythmia.
Evidence of underlying cardiovascular disease should be sought, including the sequelae of peripheral vascular disease or stroke. A healed sternal incision is obvious evidence of previous cardiothoracic surgery. A pacemaker or defibrillator, if present, can typically be palpated in the left or, less commonly, right pectoral area below the clavicle, although some older devices are found in the anterior abdominal wall or subaxillary region.
An important objective of the physical examination in the stable patient is to attempt to document the presence of AV dissociation. The presence of AV dissociation strongly suggests VT, although its absence is less helpful. AV dissociation, when present, is typically diagnosed on ECG; however, it can produce a number of characteristic findings on physical examination. Intermittent cannon A waves may be observed on examination of the jugular pulsation in the neck, and they reflect intermittent simultaneous atrial and ventricular contraction. Cannon A waves must be distinguished from the continuous and regular prominent A waves seen during some SVTs. Such prominent waves result from simultaneous atrial and ventricular contraction occurring with every beat. In addition, highly inconsistent fluctuations in the blood pressure can occur because of the variability in the degree of LA contribution to LV filling, stroke volume, and cardiac output. Moreover, variability in the occurrence and intensity of heart sounds (especially S 1 ) can also be observed and is heard more frequently when the rate of the tachycardia is slower.
The response to carotid sinus massage can suggest the cause of the WCT. The heart rate during sinus tachycardia and automatic AT will gradually slow with carotid sinus massage and then accelerate on release. The ventricular rate during AT and AFL can transiently slow with carotid sinus massage because of slowing and block of atrioventricular node (AVN) conduction. The arrhythmia itself, however, is unaffected. Atrioventricular nodal reentrant tachycardia (AVNRT) and AVRT will either terminate or remain unaltered with carotid sinus massage. VTs are generally unaffected by carotid sinus massage, although this maneuver can potentially slow the atrial rate and, in some cases, expose AV dissociation. Some VTs, such as idiopathic VT from the RV outflow tract, can infrequently terminate in response to carotid sinus massage.
Laboratory Testing
The plasma potassium and magnesium concentrations should be measured as part of the laboratory evaluation. Hypokalemia and hypomagnesemia can predispose to the development of ventricular tachyarrhythmias; however, correction of abnormalities of electrolytes is never sufficient for therapy. Hyperkalemia can cause a wide QRS complex rhythm, usually with a slow rate, with loss of a detectable P wave (the putative sinoventricular rhythm; eFig. 21.1 ) or abnormalities of AVN conduction. In patients taking digoxin, quinidine, or procainamide, plasma concentrations of these drugs should be measured to assist in evaluating possible drug toxicity.
Pharmacological Intervention
The administration of certain drugs can be useful for diagnostic, as opposed to therapeutic, purposes. Termination of the arrhythmia with lidocaine suggests, but does not prove, that VT is the mechanism. Infrequently an SVT, especially AVRT, can terminate with lidocaine. On the other hand, termination of the tachycardia with procainamide or amiodarone does not distinguish between VT and SVT. Termination of the arrhythmia with digoxin, verapamil, diltiazem, or adenosine strongly implies SVT. However, VT can also occasionally terminate after the administration of these drugs.
Unless the cause for the WCT is definitely established, however, verapamil and diltiazem should not be administered because they have been reported to cause severe hemodynamic deterioration in patients with VT and can even provoke VF and cardiac arrest. Adenosine is suggested in the 2010 Adult Advanced Cardiac Life Support (ACLS) guidelines if a WCT is monomorphic, regular, and hemodynamically tolerated, because adenosine may help convert the rhythm to sinus and may help in the diagnosis. When doubt exists, it is safest to assume any WCT is VT, particularly in patients with known cardiovascular disease. Direct current cardioversion in unstable patients and IV procainamide or amiodarone in hemodynamically stable patients are the appropriate management approach.
Electrocardiographic Features
Ventricular Tachycardia Versus Aberrantly Conducted Supraventricular Tachycardia
Because the diagnosis of a WCT cannot always be made with complete certainty, the unknown rhythm should be presumed to be VT in the absence of contrary evidence. This conclusion is appropriate both because VT accounts for up to 80% of cases of WCT and because making this assumption guards against inappropriate and potentially dangerous therapy. As noted, the IV administration of drugs used for the treatment of SVT (verapamil, diltiazem, or beta-blockers) can cause severe hemodynamic deterioration in patients with VT and can even provoke VF and cardiac arrest. Therefore these drugs should not be used when the diagnosis is uncertain.
In general, most WCTs can be classified as having one of two patterns: right bundle branch block (RBBB)–like pattern (QRS polarity is predominantly positive in leads V 1 and V 2 ), or left bundle branch block (LBBB)–like pattern (QRS polarity is predominantly negative in leads V 1 and V 2 ). The determination that the WCT has an RBBB-like pattern or an LBBB-like pattern does not, by itself, assist in making a diagnosis; however, this assessment should be made initially because it has further implications for evaluating several other features on the ECG, including the QRS axis, the QRS duration, and the QRS morphology ( Box 21.1 ; Fig. 21.2 ).
AV Relationship
- •
Dissociated P waves
- •
Fusion beats
- •
Capture beats
- •
A/V ratio <1
QRS Duration
- •
>160 ms with LBBB pattern
- •
>140 ms with RBBB pattern
- •
QRS during WCT is narrower than in NSR
QRS Axis
- •
Shift of >40 degrees between NSR and WCT
- •
Right superior (northwest) axis (−90 degrees to ±180 degrees)
- •
Left axis deviation with RBBB morphology
- •
Right axis deviation with LBBB morphology
Precordial QRS Concordance
- •
Positive concordance
- •
Negative concordance
QRS Morphology
- •
Contralateral BBB in WCT and NSR
- •
Absence of RS patterns in all precordial leads
- •
RS interval >100 ms in precordial leads with an RS morphology
- •
Lead II R wave peak time ≥50 ms
- •
Criteria in lead aVR:
- •
Presence of an initial R wave
- •
Presence of an initial r or q wave with width >40 ms
- •
Notching on the descending limb of a negative onset of a predominantly negative QRS complex
- •
V i /V t ≤ 1
- •
QRS Morphology in RBBB-Like WCT Pattern
- •
Lead V 1 :
- •
Monophasic R, biphasic qR, Rs, or Rr′ complex
- •
Broad initial R wave (≥40 msec)
- •
Rabbit ear sign: Double-peaked R wave with the left peak taller than the right peak
- •
- •
Lead V 6 :
- •
rS, QS, QR, or R complex
- •
R/S ratio <1
- •
QRS Morphology in LBBB-Like WCT Pattern
- •
Lead V 1 /V 2 :
- •
Broad initial R wave (≥30 msec)
- •
RS interval >70 msec
- •
R wave during WCT taller than the R wave during NSR
- •
Slow descent to the nadir of the S (notching in the downstroke of the S wave)
- •
- •
Lead V 6 :
- •
Any Q wave or QS complex
- •
AV, Atrioventricular; BBB, bundle branch block; LBBB, left bundle branch block; NSR, normal sinus rhythm; RBBB, right bundle branch block; WCT, wide complex tachycardia.
Rate
The rate of the WCT is of limited value in distinguishing VT from SVT because there is wide overlap in the distribution of heart rates for SVT and VT. When the rate is around 150 beats/min, AFL with 2 : 1 AV conduction and aberrancy should be considered.
Regularity
Regularity of the WCT is not helpful in distinguishing VT from SVT because, in general, both are regular. However, VT is often associated with slight irregularity of the RR intervals, QRS morphology, and ST-T waves. Although marked irregularity strongly suggests AF, VTs can be particularly irregular within the first 30 seconds of onset and in patients treated with antiarrhythmic drugs.
Atrioventricular Dissociation
AV dissociation is characterized by atrial activity (P waves) that is completely independent of ventricular activity (QRS complexes). The atrial rate is usually slower than the ventricular rate ( Fig. 21.3 ). A regular R-R interval in the presence of AF would most likely be AV dissociated.
AV dissociation is the hallmark of VT (specificity is almost 100%). However, although the presence of AV dissociation establishes VT as the cause, its absence (because of retrograde atrial capture) is not as helpful (sensitivity is 20% to 50%). AV dissociation can be present but not obvious on the surface ECG because of rapid ventricular rates. In addition, AV dissociation is absent in a large subset of VTs (especially those at a slower rate); in fact, approximately 30% of VTs have 1 : 1 retrograde VA conduction (see Fig. 21.2 ) and an additional 15% to 20% have second-degree (2 : 1 or Wenckebach) VA block ( Fig. 21.4 ). Furthermore, AV dissociation can be observed during subatrial SVT, such as junctional ectopic tachycardia and nodofascicular reentrant tachycardia.
Several ECG findings are helpful in establishing the presence of AV dissociation, including the presence of dissociated P waves, fusion beats, or capture beats.
Dissociated P waves.
When the P waves can be clearly seen and the atrial rate is unrelated to and slower than the ventricular rate, AV dissociation consistent with VT is present ( Fig. 21.5 ). An atrial rate faster than the ventricular rate is more often seen with SVTs having AV conduction block. However, during a WCT, the P waves are often difficult to identify; they can be superimposed on the ST segment or T wave (resulting in altered morphology). Sometimes the T waves and initial or terminal portions of the QRS complex can resemble atrial activity and be mistaken for P waves. If the P waves are not obvious on the ECG, several alternative leads or modalities can help in their identification, including a modified chest lead placement (Lewis leads), an esophageal lead (using an electrode wire or nasogastric tube), RA recording (obtained by an electrode catheter in the RA), carotid sinus pressure (to slow VA conduction and therefore change the atrial rate in the case of VT), or invasive EP testing.
Fusion beats.
Ventricular fusion occurs when a ventricular ectopic beat and a supraventricular beat (conducted via the AVN and HPS) simultaneously activate the ventricular myocardium. The resulting QRS complex has a morphology intermediate between the appearance of a sinus QRS complex and that of a purely ventricular complex. Intermittent fusion beats during a WCT are diagnostic of AV dissociation and therefore of VT (see Fig. 21.5 ). However, it is also possible for PVCs during SVT with aberration to produce fusion beats, which would erroneously be interpreted as evidence of AV dissociation and VT.
Capture beats.
A capture beat (once called “Dressler beat”) is a normal QRS complex, identical to the sinus QRS complex, occurring during the VT at a rate faster than the VT. The term capture beat indicates that the normal conduction system has momentarily captured control of ventricular activation from the VT focus (see Fig. 21.5 ). Fusion and capture beats are more commonly seen when the tachycardia rate is slower. These beats do not alter the rate of the VT, although a change in the preceding and subsequent RR intervals is frequently observed.
QRS Duration
In general, a wider QRS duration favors VT. In the setting of RBBB-like WCT, a QRS duration more than 140 milliseconds suggests VT, whereas for LBBB-like WCT, a QRS duration more than 160 milliseconds suggests VT. In an analysis of several studies, a QRS duration more than 160 milliseconds overall was a strong indicator of VT (likelihood ratio greater than 20 : 1). On the other hand, a QRS duration less than 140 milliseconds is not helpful for excluding VT because VT can sometimes be associated with a relatively narrow QRS complex, especially if it originates from the septum.
A QRS duration more than 160 milliseconds is not helpful in identifying VT in several settings including: (1) preexisting BBB, although it is uncommon for the QRS to be wider than 160 milliseconds in this situation; (2) preexcited SVT ( see Chapter 18 ); and (3) the presence of drugs capable of slowing intraventricular conduction (e.g., class IA and IC drugs). Of note, a QRS complex that is narrower during WCT than during normal sinus rhythm (NSR) suggests VT. However, this is rare, occurring in less than 1% of VTs.
Rarely (4% in one series), VT can have a relatively narrow QRS duration (less than 120 to 140 milliseconds). This can be observed in VTs of septal origin or those with early penetration into the HPS, as occurs with fascicular (verapamil-sensitive) VT.
QRS Axis
In general, the more leftward the axis, the greater the likelihood of VT. In addition, a significant axis shift (more than 40 degrees) between the baseline NSR and WCT is suggestive of VT (see Fig. 21.2A ). Also, a right superior (“northwest”) axis (axis from −90 degrees to ±180 degrees) is rare in SVT and strongly suggests VT (sensitivity 20%, specificity 96%; see Fig. 21.2B ).
In a patient with an RBBB-like WCT, a QRS axis to the left of −30 degrees suggests VT (see Fig. 21.2A ), and in a patient with an LBBB-like WCT, a QRS axis to the right of +90 degrees suggests VT. Furthermore, RBBB with a normal axis is uncommon in VT (less than 3%) and is suggestive of SVT.
Precordial QRS Concordance
Concordance is present when the QRS complexes in the six precordial leads (V 1 through V 6 ) are either all positive in polarity (tall R waves) or all negative in polarity (deep QS complexes). Negative concordance is strongly suggestive of VT (see Fig. 21.2D ). 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 caused by VT (see Fig. 21.2A ); however, this pattern may also be caused by preexcited SVT using a left posterior BT. Although the presence of precordial QRS concordance strongly suggests VT (greater than 90% specificity), its absence is not helpful diagnostically (approximately 20% sensitivity).
QRS Morphology
As a general rule, if the WCT is caused by SVT with aberration, then the QRS complex during the WCT must be compatible with some form of BBB that could result in that QRS configuration. If there is no combination of bundle branch or fascicular blocks that could result in such a QRS configuration, then the diagnosis, by default, is VT or preexcited SVT. As noted, WCTs can be classified as having RBBB-like pattern or LBBB-like pattern. Certain features of the QRS complex have been described that favor VT in RBBB-like or LBBB-like WCTs ( Fig. 21.6 ).
