Causes of Wide Complex Tachycardias

A narrow QRS complex requires rapid, highly synchronous electrical activation of the right ventricular (RV) and left ventricular (LV) myocardium, 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 may be fixed and present at all heart rates, or they may 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).¹

Wide QRS 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 (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 antidromic atrioventricular reentrant tachycardia (AVRT) account for 1% to 6% of WCTs.

TABLE 21-1 Causes of Wide QRS Complex Tachycardia

AT = atrial tachycardia; AVNRT = atrioventricular nodal reentrant tachycardia; AVRT = atrioventricular reentrant tachycardia; BBB = bundle branch block; BT = bypass tract; SVT = supraventricular tachycardia; VT = ventricular tachycardia.

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 useful information.²

Clinical History

Physical Examination

Most of the elements of the physical examination, including the blood pressure and heart rate, are of importance primarily in determining how severe the patient’s hemodynamic instability is 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.

An important objective of the physical examination in the stable patient is to attempt to document the presence of atrioventricular (AV) dissociation. AV dissociation is present, although not always evident, in approximately 20% to 50% of patients with VT, but it is very rarely seen in SVT. Thus, the presence of AV dissociation strongly suggests VT, although its absence is less helpful. AV dissociation, if 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 simultaneous atrial and ventricular contraction; contraction of the right atrium (RA) against a closed tricuspid valve produces a transient increase in RA and jugular venous pressure. 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. Additionally, highly inconsistent fluctuations in the blood pressure can occur because of the variability in the degree of left atrial (LA) contribution to LV filling, stroke volume, and cardiac output. Moreover, variability in the occurrence and intensity of heart sounds (especially S₁) can also be observed and is heard more frequently when the rate of the tachycardia is slower.²

The response to carotid sinus massage can suggest the cause of the WCT. The heart rate during sinus tachycardia and automatic atrial tachycardia (AT) will gradually slow with carotid sinus massage and then accelerate on release. The ventricular rate during AT and atrial flutter (AFL) can transiently slow with carotid sinus massage because of increased atrioventricular node (AVN) blockade. The arrhythmia itself, however, is unaffected. Atrioventricular reentrant nodal tachycardia (AVRNT) and AVRT will either terminate or remain unaltered with carotid sinus massage. VTs are generally unaffected by carotid sinus massage, although this maneuver may slow the atrial rate and, in some cases, expose AV dissociation. Some VTs, such as idiopathic outflow tract VT, can rarely terminate in response to carotid sinus massage.

Laboratory Tests

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. Hyperkalemia can cause a wide QRS complex rhythm, usually with a slow rate, with loss of a detectable P wave (the so-called sinoventricular rhythm; Fig. 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.

FIGURE 21-1 Wide QRS complex rhythm caused by hyperkalemia. No P waves are visible.

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, diltiazem, and probably adenosine should not be administered, because they have been reported to cause severe hemodynamic deterioration in patients with VT and can even provoke ventricular fibrillation (VF) and cardiac arrest. Direct current (DC) cardioversion in unstable patients and intravenous procainamide or amiodarone in hemodynamically stable patients are the appropriate management approach.²

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 intravenous administration of drugs used for the treatment of SVT (verapamil, adenosine, 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: a right bundle branch block (RBBB)–like pattern (QRS polarity is predominantly positive in leads V₁ and V₂) or a left bundle branch block (LBBB)–like pattern (QRS polarity is predominantly negative in leads V₁ and V₂). 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 is useful in evaluating several other features on the ECG, including the QRS axis, the QRS duration, and the QRS morphology (Table 21-2).

TABLE 21-2 Electrocardiographic Criteria Favoring Ventricular 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 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 atrial fibrillation (AF), VTs can be particularly irregular within the first 30 seconds of onset and in patients treated with antiarrhythmic drugs.

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 predictor of VT (likelihood ratio > 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.

A QRS duration more than 160 milliseconds is not helpful in identifying VT in several settings, including preexisting bundle branch block (BBB), although it is uncommon for the QRS to be wider than 160 milliseconds in this situation, preexcited SVT, and 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.²

Rarely (4% in one series), VT can have a relatively narrow QRS duration (<120 to 140 milliseconds). This can be observed in VTs of septal origin or those with early penetration into the His-Purkinje system (HPS), as occurs with fascicular (verapamil-sensitive) VT.

A recent report found that the QRS onset-to-peak time (also termed “R wave peak time” or “intrinsicoid deflection”) in lead II (measured from the beginning of the QRS to the first change of the polarity, independent of whether the QRS deflection is positive or negative) was significantly wider in VT compared with SVT with aberrancy, and a cutoff value of 50 milliseconds or greater identified VT with high sensitivity, specificity, and positive predictive values (93%, 99%, and 98%, respectively). However, this criterion has not been tested prospectively or validated in patients with preexisting conduction system disease, antiarrhythmic drug therapy, electrolyte imbalance, prior MI, and preexcited tachycardias. Additionally, certain types of VTs such as fascicular VT, bundle branch reentrant (BBR) VT, and septal myocardial VT, can have a shorter QRS onset-to-peak time because of their origin within or in close proximity to the His-Purkinje network.^1,3

QRS Axis

Generally, the more leftward the axis, the greater the likelihood of VT. A significant axis shift (>40 degrees) between the baseline NSR and WCT is suggestive of VT (Fig. 21-2A). A right superior (“northwest”) axis (axis from –90 degrees to ±180 degrees) is rare in SVT and strongly suggests VT (see Fig. 21-2B).²

FIGURE 21-2 Surface ECG of four different patients illustrating ECG morphology during normal sinus rhythm (NSR) versus ventricular tachycardia (VT). A, VT with right bundle branch block (RBBB) pattern, positive concordance, and long RS interval. Note the monophasic R in lead V₁ during VT and the significant shift in the frontal plane axis in VT versus NSR. B, VT with an RBBB pattern and long RS interval. Note the superior (“northwest”) frontal plane axis during VT. C, VT with a left bundle branch block (LBBB) pattern, long RS interval, and 1:1 ventriculoatrial conduction. Retrograde P waves (red arrows) are visible following the QRSs during VT. D, VT with LBBB pattern and negative concordance. Note that the second QRS (blue arrows) is a fusion between the sinus beat and the VT beat.

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. Additionally, RBBB with a normal axis is uncommon in VT (<3%) and is suggestive of SVT.

Precordial QRS Concordance

Concordance is present when the QRS complexes in the six precordial leads (V₁ through V₆) 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 (>90% specificity), its absence is not helpful diagnostically (approximately 20% sensitivity).

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. Detection of AV dissociation is obviously impossible if AF is the underlying supraventricular rhythm.

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 is not as helpful (sensitivity is 20% to 50%). AV dissociation can be present but not obvious on the surface ECG because of a rapid ventricular rate. Additionally, AV dissociation is absent in a large subset of VTs; in fact, approximately 30% of VTs have 1:1 retrograde ventriculoatrial (VA) conduction (see Fig. 21-2D) and an additional 15% to 20% have second-degree (2:1 or Wenckebach) VA block (Fig. 21-3).²

FIGURE 21-3 Ventricular tachycardia (VT) with type 1 second-degree (Wenckebach) ventriculoatrial (VA) block. The first beat is sinus with normal atrioventricular (AV) conduction. VT develops with an initially short VA interval (blue arrows), which then slightly prolongs (red arrows), and then VA block occurs (green arrows). Note that the VT has a right bundle branch block with long RS interval (in lead V₂).

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. 21-4). An atrial rate faster than the ventricular rate is more often seen with SVT 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 QRS portions can resemble atrial activity. Furthermore, artifacts can be mistaken for P waves. If the P waves are not obvious or suggested 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), a right atrial 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 electrophysiological (EP) testing.

FIGURE 21-4 Ventricular tachycardia (VT) with atrioventricular (AV) dissociation. Sustained monomorphic VT with a cycle length (CL) of 488 milliseconds with AV dissociation coexists with sinus rhythm with a CL of 616 milliseconds. The sinus P waves can be clearly seen (arrows) marching throughout the different phases of the VT QRS complexes, and the atrial rate is unrelated to and slower than the ventricular rate. Because of the relatively slow VT rate, capture (C) and fusion (F) beats are observed frequently.

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. 21-4). It is also possible for premature ventricular complexes (PVCs) during SVT with aberration to produce fusion beats, which would erroneously be interpreted as evidence of AV dissociation and VT.

Dressler Beats

A Dressler beat (capture 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. 21-4). 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 may be observed.

QRS Morphology

As a 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 an RBBB-like pattern or an LBBB-like pattern. Certain features of the QRS complex have been described that favor VT in RBBB-like or LBBB-like WCTs (Fig. 21-5).²

FIGURE 21-5 Diagrammatic representation of common QRS morphologies encountered in ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberration in leads V₁ and V₆ for both left bundle branch block (LBBB) and right bundle branch block (RBBB) patterns. Note the initial portions of the QRS complex in normal and aberrant QRS complexes, contrasted with the initial QRS forces in VT complexes. The RS configurations can be designated as an RBBB or LBBB type (grouped with LBBB-type morphologies).

(From Miller JM, Das MK, Arora R, Alberte-Lista C: Differential diagnosis of wide QRS complex tachycardia. In Zipes DP, Jalife J, editors: Cardiac electrophysiology: from cell to bedside, ed 4, Philadelphia, 2004, WB Saunders, pp 747-757.)

In the patient with a WCT and positive QRS polarity in lead V₁ (RBBB pattern), a monophasic R, biphasic qR complex, or broad R (>40 milliseconds) in lead V₁ favors VT (Fig. 21-6), whereas a triphasic RSR′, rSr′, rR′, or rSR′ complex in lead V₁ favors SVT (where the capital letter indicates large-wave amplitude, duration, or both; and the lowercase letter indicates small-wave amplitude, duration, or both; see Fig. 21-5). Additionally, a double-peaked R wave in lead V₁ favors VT if the left peak is taller than the right peak (the so-called rabbit ear sign; likelihood ratio > 50:1). A taller right rabbit ear does not help in distinguishing SVT from VT. On the other hand, an rS complex in lead V₆ is a strong predictor of VT (likelihood ratio > 50:1), whereas an Rs complex in lead V₆ favors SVT (see Fig. 21-6).

FIGURE 21-6 Surface ECG of four different patients illustrating ECG morphology during normal sinus rhythm (NSR) with bundle branch block (BBB) versus ventricular tachycardia (VT). A, NSR with right bundle branch block (RBBB) and VT with RBBB pattern. Note the loss of the initial r wave in V₁ and the larger S wave in V₆ during VT compared with NSR with RBBB. Additionally, note the shift in the frontal plane QRS axis from +90 degrees during NSR with RBBB to the northwest quadrant during VT. B, NSR with RBBB and VT with RBBB pattern. Note the change in QRS morphology in lead V₁ (from rsR during NSR with RBBB to monophasic R during VT) and lead V₆ (from RS during NSR with RBBB to QS during VT). Additionally, no RS complexes are observed in the precordial leads during VT. C, NSR with LBBB and VT with RBBB pattern. Note the positive precordial concordance during VT. D, NSR with LBBB and VT with RBBB pattern. Note the positive precordial concordance during VT. The second QRS (blue arrows) is a fusion between the sinus beat and the VT beat, and the fusion QRS is narrower than both the sinus and VT complexes.

In the patient with a WCT and a negative QRS polarity in lead V₁ (LBBB pattern), a broad initial R wave of 40 milliseconds or more in lead V₁ or V₂ favors VT, whereas the absence of an initial R wave (or a small initial R wave of < 40 milliseconds) in lead V₁ or V₂ favors SVT (see Fig. 21-6). Additionally, an R wave in lead V₁ during a WCT taller than that during NSR favors VT. Furthermore, a slow descent to the nadir of the S wave, notching in the downstroke of the S wave, or an RS interval (from the onset of the QRS complex to the nadir of the S wave) of more than 70 milliseconds in lead V₁ or V₂ favors VT. In contrast, a swift, smooth downstroke of the S wave in lead V₁ or V₂ with an RS interval of less than 70 milliseconds favors SVT. In an analysis of several studies, the presence of any of these three criteria in lead V₁ (broad R wave, slurred or notched downstroke of the S wave, and delayed nadir of S wave) was a strong predictor of VT (likelihood ratio > 50:1). The QRS morphology in lead V₆ is also of value; the presence of any Q or QS wave in lead V₆ favors VT (likelihood ratio > 50:1; see Fig. 21-2D), whereas the absence of a Q wave in lead V₆ favors SVT.

When an old 12-lead surface ECG is available, comparison of the QRS morphology during NSR and WCT is helpful. Contralateral BBB in WCT and NSR strongly favors VT (see Fig. 21-6C and D). It is important to note that identical QRS morphology during NSR and WCT, although strongly suggestive of SVT, can also occur in bundle branch reentrant (BBR) and interfascicular reentrant VTs.

Unfortunately, the value of QRS morphological criteria in the diagnosis of a WCT is subject to several limitations. Most of the associations between the QRS morphology and tachycardia origin are based on statistical correlations, with substantial overlap. Moreover, most of the morphological criteria favoring VT are also present in a substantial number of patients with intraventricular conduction delay present during sinus rhythm, limiting their applicability in these cases. Additionally, morphological criteria tend to misclassify SVTs with preexcitation as VT. However, preexcitation is an uncommon cause of WCT (1% to 6% in most series), particularly if other factors (e.g., age, history) suggest another diagnosis.

Variation in QRS and ST-T Morphology

Subtle, non–rate-related fluctuations or variations in the QRS and ST-T wave configuration suggest VT and reflect variations in the VT reentrant circuit within the myocardium. In contrast, because most SVTs follow fixed conduction pathways, they are generally characterized by complete uniformity of QRS and ST-T shape, unless the tachycardia rate changes.

Algorithm 1

The most commonly used algorithm is the so-called Brugada algorithm or Brugada criteria. The Brugada algorithm consists of four steps (Fig. 21-8). First, all precordial leads are inspected to detect the presence or absence of an RS complex (with R and S waves of any amplitude). If an RS complex cannot be identified in any precordial lead, the diagnosis of VT can be made with 100% specificity. Second, if an RS complex is clearly identified in one or more precordial leads, the interval between the onset of the R wave and the nadir of the S wave (the RS interval) is measured. The longest RS interval is considered if RS complexes are present in multiple precordial leads. If the longest RS interval is more than 100 milliseconds, the diagnosis of VT can be made with a specificity of 98% (see Fig. 21-8). Third, if the longest RS interval is less than 100 milliseconds, either VT or SVT still is possible and the presence or absence of AV dissociation must therefore be determined. Evidence of AV dissociation is 100% specific for the diagnosis of VT, but this finding has a low sensitivity. Fourth, if the RS interval is less than 100 milliseconds and AV dissociation cannot clearly be demonstrated, the QRS morphology criteria for V₁-positive and V₁-negative WCTs are considered. The QRS morphology criteria consistent with VT must be present in lead V₁ or V₂ and in lead V₆ to diagnose VT. A supraventricular origin of the tachycardia is assumed if either the V₁ and V₂ or V₆ criteria are not consistent with VT.

FIGURE 21-8 Brugada algorithm for distinguishing ventricular tachycardia (VT) from supraventricular tachycardia (SVT). As indicated in the inset, the RS interval is between the onset of the R wave and the nadir of the S wave. sens = sensitivity; spec = specificity.

(From Brugada P, Brugada J, Mont L, et al: A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex, Circulation 83:1649, 1991.)

The Brugada algorithm was originally prospectively applied to 554 patients with electrophysiologically diagnosed WCTs. The reported sensitivity and specificity were 98.7% and 96.5%, respectively. Other authors also found the Brugada criteria useful, although they reported a lower sensitivity (79% to 92%) and specificity (43% to 70%).

Algorithm 2

A newer algorithm for differential diagnosis of WCT was analyzed in 453 monomorphic WCTs recorded from 287 patients, based on the following: (1) the presence of AV dissociation; (2) the presence of an initial R wave in lead aVR; (3) QRS morphology; and (4) estimation of the initial (V_i) and terminal (V_t) ventricular activation velocity ratio (V_i/V_t), determined by measuring the voltage change on the ECG tracing during the initial 40 milliseconds (V_i) and the terminal 40 milliseconds (V_t) of the same biphasic or multiphasic QRS complex (Fig. 21-9).^4,5

FIGURE 21-9 Stepwise algorithm for distinguishing ventricular tachycardia (VT) from supraventricular tachycardia (SVT). AV = atrioventricular; BBB = bundle branch block; FB = fascicular block; V_i/V_t = ratio of initial (V_i) to terminal (V_t) ventricular activation velocity.

(From Vereckei A, Duray G, Szénási G, et al: Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia, Eur Heart J 28:589, 2007.)

This algorithm had superior overall total accuracy than that of the Brugada algorithm (90.3% versus 84.8%). The total accuracy of the fourth Brugada criterion was significantly lower (68% versus 82.2%) than that of the V_i/V_t criterion in the fourth step, accounting for most of the difference in outcome between the two methods.

The rationale proposed for the V_i/V_t criterion is that during WCT caused by SVT, the initial activation of the septum should be invariably rapid and the intraventricular conduction delay causing the wide QRS complex occurs in the mid to terminal part of the QRS. In contrast, in WCT caused by VT, there is initial slower muscle-to-muscle spread of activation until the impulse reaches the HPS, after which the rest of the ventricular muscle is more rapidly activated.

Antiarrhythmic drugs that impair conduction in the HPS, ventricular myocardium, or both (e.g., class I drugs and amiodarone) would be expected to decrease the V_i and V_t approximately to the same degree; therefore, the V_i/V_t ratio should not change significantly. Although the V_i/V_t ratio reflects the electrophysiology of many VTs, there are a number of exceptions to these criteria. First, disorders involving the myocardium locally can alter the V_i or V_t. For example, a decreased V_i with unchanged V_t can be present in the case of an SVT occurring in the presence of an anteroseptal MI, leading to the misdiagnosis of VT. Similarly, a scar situated at a late activated ventricular site can result in a decreased V_t in the presence of VT, leading to the misdiagnosis of SVT. Second, in the case of a fascicular VT, the V_i is not slower than the V_t. Third, if the exit site of the VT reentry circuit is very close to the HPS, it might result in a relatively narrow QRS complex and the slowing of the V_i can last for such a short time that it cannot be detected by the surface ECG.

Algorithm 3

The positive aVR criterion in algorithm 2 suggesting VT was further tested in 483 WCTs in 313 patients, and another algorithm based solely on QRS morphology in lead aVR was developed for distinguishing VT from SVT (Fig. 21-10).⁶ The new aVR algorithm is based solely on the principle of differences in the direction and velocity of the initial and terminal ventricular activation during WCT caused by VT and SVT. During SVT with BBB, both the initial rapid septal activation, which can be either left to right or right to left, and the later main ventricular activation wavefront proceed in a direction away from lead aVR, yielding a negative QRS complex in lead aVR. An exception to this generalization occurs in the presence of an inferior MI; an initial r wave (Rs complex) may be seen in lead aVR during NSR or SVT because of the loss of initial inferiorly directed forces. An rS complex also may be present as a normal variant in lead aVR, but with an R/S ratio less than 1. With these considerations, an initial dominant R wave should not be present in SVT with BBB, and its presence suggests VT, typically arising from the inferior or apical region of the ventricles.

FIGURE 21-10 New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. SVT = supraventricular tachycardia; V_i/V_t = ratio of initial (V_i) to terminal (V_t) ventricular activation velocity; VT = ventricular tachycardia.

(From Vereckei A, Duray G, Szénási G, et al: New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia, Heart Rhythm 5:89, 2008.)

Furthermore, VTs originating from sites other than the inferior or apical wall of the ventricles, but not showing an initial R wave in aVR, should yield a slow, initially upward vector component of variable size pointing toward lead aVR (absent in SVT), even if the main vector in these VTs points downward, yielding a totally or predominantly negative QRS in lead aVR. Thus, in VT without an initial R wave in lead aVR, the initial part of the QRS in lead aVR should be less steep because of the slower initial ventricular activation having an initially upward vector component, which may be manifested as an initial r or q wave with a width more than 40 milliseconds, a notch on the downstroke of the QRS, or a slower ventricular activation during the initial 40 milliseconds than during the terminal 40 milliseconds of the QRS (V_i/V_t ≤ 1) in lead aVR. In contrast, in SVT with BBB, the initial part of the QRS in lead aVR is steeper (fast) because of the invariably rapid septal activation going away from lead aVR, resulting in a narrow (≤40 milliseconds) initial r or q wave and V_i/V_t more than 1.⁶

The overall accuracy of the aVR algorithm was 91.5%, which is similar to algorithm 2 and superior to the Brugada algorithm (90.3% and 84.8%, respectively). The inability of the aVR algorithm to differentiate preexcited tachycardias from VTs, with the possible exception of the presence of an initial R wave in lead aVR, is a limitation of the algorithm.⁶

Baseline Observations during Normal Sinus Rhythm

The presence of preexcitation during NSR or atrial pacing suggests SVT, and the absence of preexcitation during NSR and atrial pacing excludes preexcited SVT.

Induction of Tachycardia

The mode of induction cannot distinguish between SVT and VT. Both atrial and ventricular stimulation may induce SVT or VT. VTs that can be induced with atrial pacing include verapamil-sensitive VT, adenosine-sensitive VT, and BBR VT.⁷

Tachycardia Features

Oscillation in the Tachycardia Cycle Length

Variations in the tachycardia CL (the V-V intervals) that are dictated and preceded by similar variations in the A-A or H-H intervals are suggestive of SVT with aberrancy or BBR VT (Fig. 21-12). In contrast, variations in the V-V intervals that predict the subsequent H-H interval changes are consistent with myocardial VT or preexcited SVT.

FIGURE 21-12 Intracardiac atrial (A-EGM) and ventricular (V-EGM) and shock lead electrograms stored by the implantable cardioverter-defibrillator during an episode of tachycardia with a 1:1 AV relationship. Note that variations in the tachycardia cycle length (the V-V intervals; blue double-headed arrow) are dictated and preceded by similar variations in the A-A intervals (red double-headed arrow), which is consistent with supraventricular tachycardia rather than ventricular tachycardia.

Atrioventricular Relationship

A 1:1 AV relationship can occur in VT and SVT. When the atrial rate is faster than the ventricular rate, VT is unlikely, except in the rare case of coexistent atrial and ventricular tachycardias (Fig. 21-13). In contrast, when the ventricular rate is faster than the atrial rate, VT is more likely, except for the rare case of junctional tachycardia or AVNRT with VA block in an upper common pathway.

FIGURE 21-13 Surface ECG of atrial tachycardia (AT) with a narrow QRS complex with the development of ventricular tachycardia (VT) with a left bundle branch block (LBBB)–like pattern. Although the atrial rate is faster than the ventricular rate, aberrant conduction during AT as the mechanism of the widening of the QRS can be excluded by observation of QRS morphology in lead V₆ (QS) inconsistent with LBBB aberrancy, a significant shift in the frontal plane QRS axis between AT and VT, and the presence of fusion beats (arrows). Additionally, the atrial rate continues unperturbed, whereas the ventricular rate is slightly irregular.

Diagnostic Maneuvers during Tachycardia

Atrial Pacing

The ability to entrain the WCT with atrial pacing can occur in VT and SVT. However, the ability to entrain the WCT with similar QRS morphology to that of the WCT (i.e., entrainment with concealed QRS fusion) excludes myocardial VT, but can occur in BBR VT and is typical for SVT. Additionally, atrial entrainment of WCT with manifest QRS fusion can occur in VT in the presence of a bystander BT, or in AVRT with multiple BTs, but not in antidromic AVRT without another BT, nor in SVT with aberrancy.⁹

The ability to dissociate the atrium with rapid atrial pacing without influencing the tachycardia CL (V-V interval) or QRS morphology suggests VT and excludes preexcited SVTs, AT with aberrancy, and orthodromic AVRT with aberrancy. However, it does not exclude the rare case of AVNRT with aberrancy associated with anterograde block in an upper common pathway during rapid atrial pacing.

The response to atrial overdrive pacing during WCTs with a 1:1 AV relationship can help distinguish VT from SVT. The concept is analogous to examination of the response to ventricular overdrive pacing during narrow complex tachycardia. During VT, atrial overdrive pacing at a CL 20 to 60 milliseconds shorter than the tachycardia CL with 1:1 AV conduction results in anterograde capture with changing or narrowing of the tachycardia QRS morphology. When the tachycardia resumes after cessation of pacing, the earliest event (after the last reset ventricular complex) occurs in the ventricle because the atrium is being passively driven by the ventricle during the tachycardia. This results in a “V-V-A response.” On the contrary, during antidromic AVRT or aberrantly conducted SVT, anterograde conduction occurs over a BT or AVN; and on cessation of atrial pacing, the last reset ventricular activation conducts to the atrium over the retrograde limb of the circuit, resulting in a “V-A response” and continuation of the tachycardia. This pacing maneuver is not useful when 1:1 AV conduction during atrial pacing is absent. Thus, when determining the response after atrial pacing during WCT, the presence of 1:1 VA conduction must be confirmed. Isorhythmic AV dissociation can mimic 1:1 AV conduction, especially when the pacing train is not long enough or the pacing CL is too slow. It is also important to ensure that atrial pacing does not terminate the tachycardia.^9,10

A “pseudo–V-V-A response” can occur during SVTs associated with a long AV interval during atrial pacing (Fig. 21-14). Because anterograde conduction during atrial pacing occurs through the slow AVN pathway, the AV interval can be longer than the pacing CL (A-A interval), so that the last paced P wave is followed first by the QRS complex resulting from slow AV conduction of the preceding paced atrial beat, and then by the QRS complex resulting from the last paced P wave. Careful examination of the last QRS complex that resulted from AV conduction during atrial pacing helps avoid this potential pitfall; the last reset QRS complex characteristically occurs at an R-R interval equal to the atrial pacing CL, whereas the first tachycardia QRS complex usually occurs at a different return CL. Furthermore, a “pseudo–A-V response” can theoretically occur in the setting BBR VT or in those with intra- or interfascicular reentrant VT, whereby the return atrial impulse may precede the first non-reset QRS complex.^9,10

FIGURE 21-14 Pseudo–V-V-A response to atrial overdrive pacing (at a cycle length [CL] of 340 milliseconds) during wide QRS complex tachycardia (WCT) (tachycardia CL, 360 milliseconds). The QRS morphology and His bundle–ventricular (HV) interval (45 milliseconds) during atrial pacing are similar to those during tachycardia. On cessation of pacing, the last atrial-paced beat is followed by a “V-V-A response” suggestive of ventricular tachycardia as the mechanism. However, although the last atrial-paced beat is followed by two QRS complexes, the last captured QRS complex (which characteristically occurs at an R-R interval equal to the atrial pacing CL) is actually the second one (as indicated by blue arrows) due to anterograde conduction over the slow atrioventricular (AV) nodal pathway, resulting in an AV interval longer than the pacing CL. Therefore, the actual response is a “V-A response” consistent with supraventricular tachycardia. This supraventricular tachycardia was atrioventricular nodal tachycardia with left bundle branch block aberrancy.

Ventricular Pacing

When overdrive ventricular pacing during the WCT fails to accelerate the atrial CL to the pacing CL (i.e., the ventricles are dissociated from the tachycardia), VT and AVRT are excluded, AT is the most likely diagnosis, but AVNRT is still possible (Fig. 21-15). Additionally, entrainment with manifest QRS fusion can occur in VT or AVRT but excludes AT and AVNRT, whereas entrainment with concealed fusion excludes SVT with aberrancy. Additionally, entrainment from the RV apex followed by a post-pacing interval (PPI) that is equal (within 30 milliseconds) to the tachycardia CL excludes AVNRT, AT, and myocardial VT, but can occur with BBR VT and AVRT using a right-sided BT.

FIGURE 21-15 A, Intracardiac atrial and ventricular electrograms (A-EGM and V-EGM, respectively) stored by the implantable cardioverter-defibrillator (ICD) during an episode of tachycardia at a cycle length (CL) of 290 milliseconds and a 1:1 AV relationship. The tachycardia triggered antitachycardia pacing (ATP) therapy by the ICD with a ramp of nine ventricular paced beats. ATP fails to terminate the tachycardia, which resumes at the baseline CL. B, A plot of atrial versus ventricular CLs during the tachycardia and two sequences of ramp ATP. Note that the atrial rate continues unperturbed during ventricular pacing (i.e., ventriculoatrial dissociation was evident during ATP), which excludes ventricular tachycardia and orthodromic atrioventricular reentrant tachycardia and is consistent with either atrial tachycardia or atrioventricular nodal reentrant tachycardia.