Wide-Complex Tachycardia: Ventricular Tachycardia versus Supraventricular Tachycardia

The Cleveland Clinic Cardiology Board Review, 2ed.

Roy Chung and Walid Saliba

Wide-complex tachycardia (WCT) is defined as a tachyarrhythmia with a rate >100 beats/min (bpm) and a QRS duration >120 milliseconds on a 12-lead electrocardiogram (ECG). Utilizing the ECG, the correct mechanistic diagnosis of a WCT rhythm is often difficult. Besides being an intellectual exercise, it is very important to establish the correct diagnosis in order to deliver appropriate acute therapy and to plan subsequent long-term patient management. Several criteria and algorithms have been developed to help distinguish among different causes of WCT. When used individually, none of these criteria reaches 100% specificity; however, when properly applied together and in conjunction with the clinical history and presentation, the algorithms serve as a guide to the correct diagnosis in the majority of the cases.

WCT can result from either a ventricular or a supraventricular mechanism. Ventricular tachycardia (VT) originates below the level of the His bundle. Supraventricular tachycardia (SVT) originates in or involves structures above the His bundle. SVT may involve atrial tachycardia, atrial fibrillation, atrial flutter, atrioventricular (AV) node reentrant tachycardia (Fig. 30.1), or AV reentrant tachycardia. AV reentrant tachycardia may be either orthodromic reentrant tachycardia or antidromic reentrant tachycardia (Fig. 30.2). Orthodromic reentrant tachycardia occurs when antegrade ventricular conduction occurs via the AV node and retrograde conduction to the atrium is via the accessory pathway. Antidromic reentrant tachycardia occurs when ventricular antegrade conduction occurs over the accessory pathway and retrograde conduction occurs via the AV node.

FIGURE 30.1 Supraventricular tachycardia.

FIGURE 30.2 AV reentrant tachycardia.

DIFFERENTIAL DIAGNOSIS

WCT can occur by three different mechanisms:

1. VT is the most common cause of WCT in the general population, accounting for >80% of all cases. It is even more common in patients with structural heart disease, and it may occur in 98% of patients with a prior history of a myocardial infarction. VT may be either monomorphic or polymorphic. Monomorphic VT occurs when the QRS morphology is stable and uniform, whereas polymorphic VT occurs when the QRS complexes vary in morphology.

2. The second mechanism of WCT occurs when the tachycardia originates above the ventricle and has abnormal ventricular activation, also known as SVT with aberrancy. It accounts for 15% to 20% of all cases of WCT and includes a variety of disorders.

a. The first example is SVT with bundle branch block aberration, which may be either a right bundle branch block (RBBB) or a left bundle branch block (LBBB) morphology (Fig. 30.3). Activation of the ventricle through the His–Purkinje system (His bundle and both bundle branches) results in a narrow QRS complex. Activation of the ventricle unilaterally via one bundle branch results in a wide QRS complex, because activation of the remainder of the ventricular myocardium is dependent on slow myocardial conduction. Aberration occurs when there are abnormalities of intraventricular conduction in response to changing heart rate, and when the conduction over the His–Purkinje conduction system is delayed or blocked in either the right or left bundle branch. RBBB is more common, occurring in 80% of cases. The aberration may be fixed, occurring in normal sinus rhythm at a slow heart rate, or it may be functional and present only during tachycardia.

FIGURE 30.3 SVT with bundle branch block.

b. SVT with antegrade conduction via an accessory pathway, such as in Wolff–Parkinson–White syndrome, accounts for 1% to 5% of all WCT. The accessory pathway is an anomalous AV connection that inserts directly into ventricular myocardium at the base of the ventricle along the mitral or tricuspid valve annulus. Ventricular activation is initiated at this insertion point and is termed ventricular pre-excitation. Pre-excited tachycardia can occur with SVT with antegrade conduction via the accessory pathway. The accessory pathway is not part of the tachycardia circuit and is not essential for its perpetuation. The other form of pre-excited tachycardia can occur with antidromic reciprocating tachycardia, in which the accessory pathway is part of the tachycardia circuit (Fig. 30.4).

FIGURE 30.4 SVT with pre-excitation.

c. Another form of WCT is SVT with an intraventricular conduction delay. This can occur in patients with cardiomyopathy, corrected congenital heart disease such as tetralogy of Fallot, or Ebstein anomaly, in which myocardial conduction is further impaired. The conduction abnormality is usually apparent during normal sinus rhythm.

d. Some medications are capable of producing nonspecific widening of the QRS complex during SVT. These include Na⁺ channel blockers, especially Class IC agents (flecainide, encainide), less so Class IA antiarrhythmics (quinidine, procainamide, disopyramide), and amiodarone. The most common example is a patient with atrial flutter being treated with flecainide. Flecainide can induce flutter rate slowing to permit 1:1 AV nodal conduction and a secondary increase in the ventricular rate with a wide QRS complex. This is as a result of the slow ventricular conduction in response to the Na⁺channel blockade. This can be easily and erroneously interpreted as VT (Fig. 30.5).

FIGURE 30.5 Atrial Flutter with 1:1 conduction.

e. Electrolyte abnormalities such as hyperkalemia can cause widening of the QRS complex and can be mistakenly interpreted as VT. The morphology is typically LBBB.

3. Ventricular paced rhythms can also mimic WCT (Fig. 30.6). Most pacemakers are dual chamber, with a lead in the right atrium and one in the right ventricle. Pacing of the right ventricle causes an LBBB QRS morphology. The surface ECG representation of the pacing stimulus is less apparent with the use of bipolar pacing modes and a resultant decrease in the energy requirement for reliable ventricular pacing. Therefore the pacing spike may be overlooked or even absent from ECG tracings. A wide QRS tachycardia can occur in any SVT with atrial tracking, in which the ventricle is paced in response to atrial sensing. In these cases, it is essential to obtain an adequate history and to analyze a previous ECG to evaluate the baseline morphology of the QRS complex.

FIGURE 30.6 Ventricular paced tachycardia.

4. Pacemaker-mediated tachycardia can also produce a WCT. The pacemaker is itself responsible for the tachycardia when ventricular pacing results in retrograde conduction to the atrium. The pacemaker senses the atrial conduction, resulting in ventricular pacing, which in turn is followed by retrograde conduction to the atrium, resulting in “endless loop tachycardia” (Fig. 30.7).

FIGURE 30.7 Ventricular paced tachycardia. Left: Atrial tracking. Right: Pacemaker-mediated tachycardia.

5. Lastly, artifacts from recording equipment problems (such as fast-sweep speed recording) or from external repetitive motion (such as brushing teeth) can present as “WCT” (Fig. 30.8).

FIGURE 30.8 Artifact mimicking WCT.

DIAGNOSIS

Clinical Presentation

In order to diagnose the etiology of the WCT, it is important to evaluate the clinical presentation. As mentioned before, obtaining an accurate patient history is crucial in formulating an accurate rhythm diagnosis. A prior history of heart disease, myocardial infarction, or congestive heart failure makes the diagnosis of VT highly suggestive as the cause of the WCT. Akhtar et al. have reported that the positive predictive value of a WCT representing VT in a patient with a prior history of myocardial infarction is 98%. Tchou reported that of patients who had a prior myocardial infarction and a first episode of tachycardia occurring after the infarction, 28 of 29 patients presented with VT and were diagnosed correctly. The older the patient is, the more likely that the tachycardia is ventricular; however there is a significant overlap with SVT patients. It is also helpful to know if there is any presence of congenital heart disease, or if the patient has a pacemaker or defibrillator. Knowing that the patient has an implantable cardioverter-defibrillator (ICD) raises a concern for pacemaker-associated tachycardia, but more important, the presence of the device suggests that the patient has risk factors for VT. A history of a prior similar episode may also be useful. The first occurrence of the arrhythmia after a myocardial infarction is highly suggestive of VT, whereas SVT may be more likely if there is recurrence of the arrhythmia over several years. The presence of other medical conditions can point to a diagnosis of WCT. For example, in a patient with renal failure, the WCT may be attributable to hyperkalemia. In a patient with known peripheral vascular disease, the WCT may be indicative of VT, because such patients are likely to have underlying coronary artery disease.

Knowing what medications the patient is taking, especially cardiac medications, is vital when evaluating WCT. It is important to identify medications that prolong the QT interval, such as dofetilide, sotalol, quinidine, and erythromycin, which can all cause torsade de pointes, a form of polymorphic VT. Electrolyte abnormalities caused by certain medications such as diuretics (hypokalemia and hypomagnesemia) or angiotensin-converting enzyme (ACE) inhibitors (hyperkalemia) may predispose to VT. Patients who are on digoxin are more susceptible to an arrhythmia when hypokalemia is present. The most common arrhythmias are monomorphic VT, bidirectional tachycardia, and junctional tachycardia, and typically occur when the plasma digoxin concentration is >2.0 ng/mL. As stated earlier, Class IC agents can cause rate-related aberrant conduction during SVT. Symptoms such as palpitations, lightheadedness, or chest pain are generally not useful in evaluating the etiology of the WCT.

One of the priorities in evaluating a patient with WCT is determining if the patient is hemodynamically stable or unstable. This requires knowing the patient’s blood pressure and heart rate. In a patient who is unstable, emergency cardioversion is required and the mechanism of the arrhythmia may not necessarily be known. VT can be present when the patient is hemodynamically stable and should not be mistaken for SVT, lest the patient be given inappropriate medical therapy (such as adenosine or verapamil) that can lead to hemodynamic compromise with VT. When the patient is hemodynamically stable, a more detailed physical exam can be performed. Inspection of the chest can point to underlying cardiovascular disease when there is a sternal incision, a pacemaker, or defibrillator.

AV dissociation occurs in 60% to 75% of patients with VT and is a result of the atria and ventricles depolarizing independently. It almost never occurs in SVT. This finding is usually identifiable on the surface ECG. However, it is also possible to make this diagnosis on physical exam by assessing the jugular venous pulsation. Cannon A waves are irregular pulsations that are of greater amplitude than the normal jugular venous waves, and occur intermittently when the atrium and ventricle contract simultaneously. When the tachycardia rate is slower, there can be variable intensity of the first heart sound. However, evaluating this may not be practical in an acute situation.

Laboratory tests should be performed for patients with WCT to determine potassium and magnesium levels. If the patient is on digoxin, it is also important to obtain the serum digoxin level. If a chest x-ray is available, one can readily identify the presence of a pacemaker, defibrillator, or sternal wires that might point to underlying structural heart disease.

Provocative Maneuvers

Certain bedside maneuvers can be performed to distinguish VT from SVT. The Valsalva maneuver or carotid sinus massage enhances vagal tone, which depresses sinus nodal and AV nodal activity. These maneuvers will slow the heart rate during sinus tachycardia, but once they are completed, the heart rate will increase again. If the patient is in SVT, these maneuvers may terminate the rhythm. If the patient is in an atrial tachycardia or flutter, the rhythm will persist though the ventricular rate may be slower, thus uncovering the background atrial activity. These maneuvers can also elicit VA conduction block, which can induce AV dissociation during VT.

Certain medications can be used to diagnose the tachyarrhythmias. For example, adenosine, given in 6- to 12-mg boluses intravenously during WCT, can result in one of the following scenarios:

1. The tachycardia terminates, making it more likely to be supraventricular in etiology, invoking AV node participation. Some atrial tachycardias may also terminate with adenosine.

2. AV block occurs, uncovering the background atrial activity such as atrial tachycardia, flutter, or fibrillation, thus allowing the diagnosis of an atrial tachyarrhythmia.

3. If 1:1 AV association is present and evident during WCT, adenosine-induced AV block results in AV dissociation, thus making the diagnosis VT

Adenosine has a short half-life of about 10 seconds. However, it has to be used with caution, because it may cause hemodynamic compromise in a patient with VT. Some paroxysmal VT in structurally normal hearts may terminate with adenosine.

Termination of the rhythm with lidocaine suggests VT as the mechanism. Amiodarone and procainamide, however, will not diagnose the rhythm if the WCT is terminated. Beta-blockers may be given as well. They can terminate SVT or uncover AV dissociation during VT in a manner similar to adenosine. It is important that verapamil not be given if the diagnosis is in question, because it can lead to significant hemodynamic compromise in VT and induce ventricular fibrillation and cardiac arrest.

ECG Criteria

The most reliable way to differentiate VT from SVT is by evaluating the ECG. A 12-lead ECG is more helpful than a rhythm strip. A rhythm strip may be additive as a result of analyzing the beginning and termination of the tachycardia. A previous ECG during a normal rhythm will help to identify the baseline QRS morphology and the presence of Q waves that might suggest a prior myocardial infarction. Ventricular pre-excitation may be suggested if there is the presence of delta waves.

There are several ECG criteria and different algorithms that may be used to differentiate VT from SVT in WCT:

1. The tachycardia rate has no diagnostic value in determining the mechanism of the WCT.

2. Regularity of the RR intervals is also not a useful criterion, because VT can be irregular in patients on antiarrhythmic medications.

3. QRS-complex duration can be useful in differentiating VT from SVT. The WCT is more suggestive of VT when the QRS duration is >140 milliseconds with an RBBB morphology and >160 milliseconds with an LBBB morphology. A study by Wellens showed that all of 70 patients with WCT due to SVT had QRS-complex durations <140 milliseconds, whereas 66% of patients with WCT due to VT had QRS-complex duration >140 milliseconds. Another study, by Akhtar, showed that 15% of patients with VT had QRS-complex duration <140 milliseconds and that QRS duration >140 milliseconds with RBBB pattern or >160 milliseconds with LBBB pattern correlates with VT. Wide QRS-complex duration can still be seen with pre-excitation, ventricular pacing, use of antiarrhythmic drugs, and marked baseline intraventricular conduction delays. VT in structurally normal hearts may have a relatively narrow QRS complex in a case with idiopathic left ventricular VT.

4. The QRS-complex axis may also be helpful in diagnosing WCT. A right superior QRS-complex axis in the frontal plane is more suggestive of VT. Presence of LBBB and right-axis deviation is also almost always due to VT. Presence of Q waves that are also present in normal sinus rhythm suggests prior myocardial infarction, which makes the diagnosis of VT more likely. Pseudo-Q waves can be seen in SVT, which represents retrograde atrial activation.

5. QRS-complex concordance in the precordial leads is highly predictive of VT, with a specificity as high as 90% or greater. The sensitivity is low because it is only present in <20% of patients with VT. Concordance occurs when all the QRS complexes in the precordial leads (V₁ to V₆) have the same polarity, either positive or negative (Fig. 30.9). It is important to remember that 1% to 2% of patients with pre-excited tachycardia involving left lateral accessory pathways possess positive QRS-complex concordance.

FIGURE 30.9 VT: QRS concordance.

6. AV dissociation is the most useful criterion to distinguish VT from SVT (Fig. 30.10). It occurs in up to 60% of patients with VT but is apparent on the surface ECG in only 20% to 30% of patients. The specificity is 99%, but again, the sensitivity is only 20%. AV dissociation occurs in <1% of all SVTs. Several methods can be used to maximize atrial recordings, such as using an esophageal lead, utilizing temporary epicardial atrial pacemaker wires post–cardiac surgery, changing arm lead position, and utilizing a pacemaker programmer for atrial and ventricular electrogram display in patients with permanent dual-chamber devices. Thirty percent of VT patients may have 1:1 AV association, and this cannot be differentiated from SVT. Transient AV dissociation can be elicited with carotid sinus massage or IV adenosine, which helps to confirm the diagnosis of VT.

FIGURE 30.10 VT: AV dissociation.

7. The presence of capture and fusion complexes on an ECG during WCT makes the diagnosis of VT more likely. A ventricular fusion complex results from simultaneous activation of the ventricle by two or more impulses originating from the same or different chambers of the heart. An example is the fusion of a ventricular impulse with a sinus or other supraventricular conducted impulse, or another ventricular impulse. The resulting QRS-complex morphology is variable and depends on the relative contribution of each of the sources of ventricular activation. During WCT, a change in the morphology of the QRS complex is indicative of fusion and suggests the diagnosis of VT. A fusion complex is not pathognomonic for VT and can occur when a premature ventricular contraction occurs during SVT with aberrancy. A capture complex is a ventricular QRS complex that results from conduction of a supraventricular impulse to the ventricle and ventricular depolarization before the ventricle is depolarized by the VT circuit. It is usually a narrower complex and is identical to the sinus QRS complex. It indicates that the normal conduction system has temporarily captured and depolarized the ventricle before the next VT complex. Although fusion and capture complex are seen infrequently, when they are present, they strongly indicate the etiology of WCT as VT, with the specificity being 99% and the sensitivity 5% for capture complex (Fig. 30.11A,B).

FIGURE 30.11 A: Fusion complex. B: Fusion and capture complexes.

8. The absence of a precordial RS pattern on a 12-lead ECG is suggestive of VT. This is the first criterion in Brugada’s algorithm. Brugada performed an analysis on 554 patients with WCT. Fifteen percent of all cases had an absent RS pattern, and 100% of these cases were due to VT. Though the specificity remains high (100%), the sensitivity is quite low (21%). If an RS pattern is present, an RS duration (as measured from the beginning of the R wave to the nadir of the S wave) of >100 milliseconds suggests VT (Fig. 30.12). This is the second step in Brugada’s algorithm. This finding is present in 32% of patients with WCT and has a specificity of 98%. Combining these two criteria can correctly diagnose 47% of all WCT and identify 66% of all VT.

FIGURE 30.12 RS.

9. QRS morphology: Different criteria for RBBB and LBBB morphologies can also help distinguish VT from SVT (Table 30.1; Fig. 30.13). This is based predominantly on the QRS-complex analysis in the precordial leads: V₁, V₂, and V₆. If the QRS complex is predominantly positive in V₁, a “RBBB-like” pattern is observed and the corresponding morphology criteria are applied. Alternatively, if the QRS complex is predominantly negative in V₁, a “LBBB-like” pattern is observed and the corresponding morphology criteria are applied.

TABLE

30.1 Morphology Criteria

FIGURE 30.13 Morphology criteria.

ALGORITHMS

The most commonly used approach for the differential diagnosis of WCT is the aforementioned algorithm by Brugada (Fig. 30.14). This algorithm is comprised of four steps and has a sensitivity of 98.7% and a specificity of 96.5%. The four sequential steps assess for the presence of RS QRS complexes in the precordial leads, the RS interval, AV dissociation, and specific morphology criteria for VT in V₁ and V₆(Fig. 30.15).

FIGURE 30.14 Brugada’s criteria I.

FIGURE 30.15 This ECG shows an RS pattern in V₁ to V₅. The RS interval measures 140 milliseconds in V₄, which suggests a diagnosis of VT with 98% specificity.

A second-level algorithm (Brugada’s criteria II) helps to distinguish VT from pre-excited SVT. This algorithm has three steps and has a sensitivity of 75% and specificity of 100% Figs. 30.16 and 30.17).

FIGURE 30.16 Brugada’s criteria II.

FIGURE 30.17 ECG: AV dissociation.

SPECIAL CASES

There are other miscellaneous ECG criteria that can help differentiate VT from SVT:

When the QRS complex during WCT is narrower than in normal sinus rhythm, it is more suggestive of VT.

The WCT is more likely to be VT if there is contralateral bundle branch block in normal sinus rhythm rather than during the WCT.

Although regularity in itself does not help to distinguish SVT from VT, rapid irregular WCT with beat-to-beat QRS-duration variation is suggestive of atrial fibrillation with WPW (Fig. 30.18)

Misdiagnosis of SVT as VT using morphology criteria can occur when the WCT is a result of pre-excited tachycardia or a paced ventricular rhythm.

VT can be misdiagnosed as SVT in cases of bundle branch reentrant VT (BBR-VT). This occurs when ventricular activation begins via the RBBB and produces a LBBB QRS morphology. The conduction spreads transseptally to retrogradely, reentering the LBBB and establishing the reentry circuit of BBR-VT. Following the morphology criteria for LBBB QRS complexes will lead to an incorrect diagnosis of SVT with LBBB aberrancy. However, if AV dissociation is present, the correct diagnosis of VT will be made.

A narrow QRS VT can occur with QRS durations <140 milliseconds. This can occur in 12% of VTs. A possible explanation is when the origin of the VT comes from the septum, which causes simultaneous spread of ventricular activation. Such is the case when idiopathic left VT (fascicular VT) is present. This type of VT can be terminated with IV verapamil and is therefore misdiagnosed as SVT.

FIGURE 30.18 Examples of other ECG criteria.

CONCLUSIONS

Despite multiple diagnostic tools, the determination of WCT etiology can be difficult. Morphology criteria are difficult to remember with certainty. The widespread use of antiarrhythmic medications with secondary intraventricular conduction delay has reduced the accuracy of currently available algorithms. Certain key points that should be committed to memory:

If the configuration of the WCT is not compatible with aberration, then it is likely to be VT.

If structural heart disease is present, WCT is most likely VT.

Certain type of treatments (verapamil, adenosine) can potentially worsen the patient’s situation. So if the diagnosis remains in question, treat it as though it is VT.

Using morphology criteria, pre-excited tachycardias and paced ventricular rhythms may be easily mistaken for VT.

AV dissociation remains the most important and most specific criterion for the diagnosis of VT.

In some situations, “I don’t know” is the correct answer. In these cases, an electrophysiology study may be necessary for an accurate arrhythmic diagnosis.

ACKNOWLEDGEMENT

The authors thank Dr. Kanderian for her contribution to the earlier edition of this chapter.

VT:	QRS >140 ms for right bundle branch block (RBBB),
	QRS >160 ms for left bundle branch block (LBBB)