Cardiology

Differential Diagnosis of Wide QRS Complex Tachycardias

I. Wide QRS Tachycardia: What every physician needs to know.

A. Wide Complex Tachycardia: Definition of Wide and Narrow

Related Topics

Aberrancy, ventricular tachycardia, supraventricular tachycardia, right-bundle branch block (RBBB), left-bundle branch block (LBBB), intraventricular conduction delay (IVCD), pre-excited tachycardia.

Definitions

The normal QRS complex during sinus rhythm is “narrow” (<120 ms) because of rapid, nearly simultaneous spread of the depolarizing wave front to virtually all parts of the ventricular endocardium, and then radial spread from endocardium to epicardium.

This is achieved by rapid propagation along the common bundle of His, the right and left bundle branches, the fascicles of the left bundle branch, and the Purkinje network. This collection of propagating structures is referred to as the “His-Purkinje network.”

A “wide QRS complex” refers to a QRS complex duration ≥120 ms. Widening of the QRS complex is related to slower spread of ventricular depolarization, either due to disease of the His-Purkinje network and/or reliance on slower, muscle-to-muscle spread of depolarization. This can be seen during:

  1. propagation of a supraventricular impulse (atrial premature depolarizations [APDs] or supraventricular tachycardia [SVT]) with block (preexisting or rate-related) in one or more parts of the His-Purkinje network;

  2. depolarizations originating in the ventricles themselves (ventricular premature beats [VPDs] or ventricular tachycardia [VT]);

  3. slowed propagation of a supraventricular impulse because of intra-myocardial scar/fibrosis/hypertrophy; or

  4. conduction of a supraventricular impulse from atrium to ventricle over an accessory pathway (bypass tract) – so called “pre-excited” tachycardia.

II. Diagnostic Confirmation: Are you sure your patient has Wide QRS Tachycardia?

What determines the width of the QRS complex?

The clinical situation that is commonly encountered is when the clinician is faced with an electrocardiogram (ECG) that shows a wide QRS complex tachycardia (WCT, QRS duration ≥120 ms, rate ≥100 bpm), and must decide whether the rhythm is of supraventricular origin with aberrant conduction (i.e., with bundle branch block), or whether it is of ventricular origin (i.e., VT). It is important to note that all the analyses that help the clinician distinguish SVT with aberrancy from VT also help to distinguish single wide complex beats (i.e., APD with aberrant conduction vs. VPD).

The width of the QRS complex, both with aberrancy and during VT, can vary from patient to patient. Scar tissue, as seen in patient with prior myocardial infarctions or with cardiomyopathy, may further slow intramyocardial conduction, resulting in wider QRS complexes in both situations.

During VT, the width of the QRS complex is influenced by:

  1. The site of VT origin: free wall sites of origin result in wider QRS complexes due to sequential activation (in series) of the two ventricles, as compared to septal sites, which result in simultaneous activation (in parallel).

  2. The timing of engagement of the His-Purkinje network: at some point during propagation of the VT wave front, the His-Purkinje network is engaged, resulting in faster propagation; the earlier this occurs, the narrower the QRS complex. For example, VTs that arise within scar tissue located in the crest of the interventricular septum may “break into” (engage) the His bundle or proximal bundle branches early, and subsequent spread of electrical activation occurs via the His-Purkinje network, resulting in relatively narrower QRS complexes. Such VTs may look very similar to SVT with aberrancy.

  3. The “burden” of intramyocardial scar: as mentioned above, scar within the ventricles will affect the velocity of propagation through the myocardium and influence QRS complex width. In general, the presence of scar can be inferred from QRS complex “fractionation” or “splintering” or “notching."

  4. The presence of antiarrhythmic drugs (especially class Ic or class III antiarrhythmic drugs) or electrolyte abnormalities (such as hyperkalemia) can slow intra-myocardial conduction velocity and widen the QRS complex. Flecainide, a class Ic drug, is an example that is notorious for widening the QRS complex at faster heart rates, often resulting in bizarre-looking ECGs that tend to cause diagnostic confusion.

III. Management.

Systematic approach to wide complex tachycardia: historical features

As is true of all situations in medicine, the clinical context in which the wide complex tachycardia (WCT) occurs often provides important clues as to whether one is dealing with VT or SVT with aberrancy. The following historical features (Table I) powerfully influence the final diagnosis. A WCT that occurs in a patient with a history of prior myocardial infarction can be safely assumed to be VT unless proven otherwise.

Table I.

Historical features to help distinguish causes of WCT

It should be noted that hemodynamic stability is not always helpful in deciding about the probable etiology of WCT. Many patients with VT, especially younger patients with idiopathic VT or VT that is relatively slow, will not experience syncope; on the other hand, some older patients with rapid SVT (with or without aberrancy) will experience dizziness or frank syncope, especially with tachycardia onset.

A. Immediate management.

B. Physical Examination Tips to Guide Management.

Systematic approach to wide complex tachycardia: physical examination

The hallmark of VT is ventriculoatrial (VA) dissociation (the ventricular rate being faster than the atrial rate), the following examination findings (Table II), when clearly present, “clinch” the diagnosis of VT. Absence of these findings is not helpful, since VT can show VA association (1:1 VA conduction or VA Wenckebach during VT). Of course, such careful evaluation of the patient is only possible when the patient is hemodynamically stable during VT; any hemodynamic instability (such as presyncope, syncope, pulmonary edema, angina) should prompt urgent or emergent cardioversion. Therefore, measurement of vital signs and a thorough but rapid physical examination are vital in deciding on the initial approach to the patient with WCT. If the patient is conscious and cardioversion is decided upon, it is strongly recommended that sedation or anesthesia be given whenever possible prior to shock delivery.

Table II.

Findings on Physical Examination to help distinguish causes of WCT

Recognition of intermittent "cannon" A waves on the jugular venous waveform (JVP) during ongoing WCT is an important physical examination finding because it implies VA dissociation, and can clinch the diagnosis of VT. The recognition of variable intensity of the first heart sound (variable S1) can similarly be another clue to VA dissociation, and can help make the diagnosis of VT.

Systematic approach to wide complex tachycardia: ECG findings

Whenever possible, a 12-lead ECG should be obtained during WCT; obviously, this is not applicable to the hemodynamically unstable patient (such as presyncope, syncope, pulmonary edema, angina). Because of this reason, many patients have only ECG telemetry (rhythm) strips available for analysis; however, there is often sufficient information within telemetry strips to make an accurate conclusion about the nature of WCT. Capturing the onset or termination of WCT on telemetry strips can be especially helpful. On a practical matter, telemetry recordings are often erased once the patient leaves that location, and it is important to print out as many examples of the WCT as possible for future review by the cardiology or electrophysiology consultant.

General approach to the ECG showing a WCT

  1. Any WCT should be assumed to be VT until proven otherwise. Therefore, onus of proof is on the electrocardiographer to prove that the WCT is not VT.

  2. Any QRS complex morphology that does not look typical for right- or left-bundle branch block should strongly favor the diagnosis of VT.

  3. The wider the QRS complex, the more likely it is to be VT. In other words, the default diagnosis is VT, unless there is no doubt that the WCT is SVT with aberrancy.

  4. A "northwest" frontal axis during WCT strongly favors VT (since neither RBBB nor LBBB aberrancy results in such an axis).

  5. The more “splintered,” “fractionated,” or “notched” the QRS complex is during WCT, the more likely it is to be VT.

  6. Precordial concordance, when all the precordial leads show positive or negative QRS complexes, strongly favors VT (since neither RBBB nor LBBB aberrancy results in such concordance).

  7. Comparison of the QRS complex to a prior ECG in sinus rhythm is most helpful; a virtually identical (wide) QRS in sinus rhythm favors a supraventricular tachycardia with preexisting aberrancy.

  8. When a WCT abruptly becomes a narrow complex tachycardia with acceleration of the heart rate, SVT (orthodromic atrioventricular reciprocating tachycardia using an accessory pathway on the same side as the blocked bundle branch) is confirmed (Coumel’s law).

  9. When a WCT abruptly becomes a narrow QRS rhythm at exactly half the rate of the WCT, atrial flutter with 1:1 AV conduction transitioning to 2:1 AV conduction is very likely (i.e., SVT with aberrancy).

  10. When VT occurs in patients with prior myocardial infarction, the QRS complex during VT shows “pathologic Q waves” in the same leads that showed pathologic Q waves in sinus rhythm. In other words, the VT morphology shows the infarct location because VT most often arises from the infarct scar location. Therefore, the finding of deep Q waves during a WCT favors VT.

  11. Often, single wide complex beats that are clearly VPDs may be present during sinus rhythm on prior ECGs or other rhythm strips; if the QRS complex morphology of the WCT is identical to that of the VPDs, VT is likely.

  12. It must be acknowledged that there are many clinical scenarios where different criteria will provide conflicting indications as to the etiology of a WCT. Such confusion is most often related to the occasional patient where aberrancy results in a particularly bizarre QRS complex morphology, raising the likelihood that the WCT might be VT. This is where the experienced electrocardiographer must weigh the conflicting indicators and reach a clinical decision. In an effort to aid the clinician, scoring systems have been recently proposed, but their clinical performance is only marginally superior to older criteria (see references).

  13. In the hemodynamically stable patient, obtaining an ECG with specially located surface ECG electrodes can be helpful in recognizing dissociated P waves. One such special lead is called the “modified Lewis lead”; the right arm electrode is intentionally placed on the second right intercostal space, and the left arm electrode on the fourth right intercostal space. Such a re-orientation of lead I electrodes so that they “straddle” the right atrium, often allows more accurate recognition of atrial activity, and if dissociated P waves are seen, the diagnosis of VT is established.

  14. Evidence of “fusion beats” or capture beats” is evidence for VA dissociation, and clinches the diagnosis of VT. ECG evidence of even a single dissociated P wave at the onset of tachycardia (i.e., AV dissociation at the onset) may be sufficient evidence on a telemetry strip to recognize VT.

Table III shows general ECG findings that help distinguish SVT with aberrancy from VT.

Table III.

General ECG findings that help distinguish SVT with aberrancy from VT

C. Laboratory Tests to Monitor Response to, and Adjustments in, Management.

Special situations with wide complex tachycardia

Wide complex tachycardia related to preexcitation

A special consideration is WCT due to anterograde conduction over an accessory pathway. One such example would be antidromic atrioventricular reciprocating tachycardia (AVRT), where the impulse travels anterogradely (from the atrium to the ventricle) over an accessory pathway (bypass tract), and then uses the normal His-Purkinje network and AV node for retrograde conduction back up to the atrium.

Because an accessory pathway inserts directly into ventricular myocardium, the resulting QRS complex during antidromic AVRT is generated by muscle-to-muscle spread propagating away from the ventricular insertion site, rather than via His-Purkinje spread, and therefore meets all the QRS complex morphology criteria for VT. This is one SVT where the QRS complex morphology exactly mimics that of VT.

However, such patients are usually young, do not have associated structural heart disease, and most importantly, show manifest preexcitation (WPW pattern) during sinus rhythm. The pattern of preexcitation in sinus rhythm (the "delta" wave) will be exactly reproduced (and exaggerated – so called "full preexcitation") during antidromic AVRT. Carotid massage and adenosine will terminate this WCT by causing transmission block in the retrograde limb (the AV node).

Wide complex tachycardia due to bundle branch reentry

Bundle branch reentry (BBR) is a special type of VT wherein the VT circuit is comprised of the right and left bundles and the myocardium of the interventricular septum. In its commonest form, the impulse travels down the RBB, across the interventricular septum, and then up one of the fascicles of the left bundle branch. Because ventricular activation occurs over the RBB, the QRS complex during this VT exactly resembles the QRS complex during SVT with LBBB aberrancy. When the direction is reversed (down the LBB, across the septum, and up the RBB), the QRS complex exactly resembles the QRS complex during SVT with RBBB aberrancy.

This is one VT where the QRS complex morphology exactly mimics that of SVT with aberrancy. However, such patients have severe, dilated cardiomyopathy, and preexisting BBB or intraventricular conduction delays (wide QRS in sinus rhythm). Furthermore, there will often be evidence of VA dissociation, with the ventricular rate being faster than the atrial rate, pointing to the correct diagnosis of VT.

Wide complex tachycardia in the setting of metabolic disorders

Electrolyte disorders (such as severe hyperkalemia) and drug toxicity (such as poisoning with antiarrhythmic drugs) can widen the QRS complex. Toxicity with flecainide, a class Ic antiarrhythmic drug with potent sodium channel blocking capabilities, is a well-known cause of bizarrely wide QRS complexes and low amplitude P waves. If the ambient sinus rate is rapid, the resulting ECG may show a WCT. Once again, the clinical scenario in which such a patient is encountered (such as history of antiarrhythmic drug use), along with other ECG findings (such as tall peaked T waves in hyperkalemia) will help make the correct diagnosis.

Wide complex tachycardia related to rapid ventricular pacing

Pacing results in a wide QRS complex since the wave front of depolarization starts in the myocardium at the ventricular lead location, and then propagates by muscle-to-muscle spread. Any cause of rapid ventricular pacing will result in result in a WCT.

If the pacing artifact (“spikes”) are not large; especially true with bipolar pacing; they may be missed. Known history of pacemaker implantation and comparison to prior ECGs usually provide the correct diagnosis. Dual-chamber pacemakers may show rapid ventricular pacing as a result of “tracking” at the upper rate limit, or as a result of pacemaker-mediated tachycardia.

IV. Management with Co-Morbidities

Examples of wide complex tachycardia

Figure 1. WCT tachycardia obtained from a 72-year-old man with a history of remote anteroseptal myocardial infarction and reduced ejection fraction.

Figure 1.

WCT tachycardia obtained from a 72-year-old man with a history of remote anteroseptal myocardial infarction and reduced ejection fraction.

The following observations can be made:

1. The QRS duration is very broad, approaching 200 ms; the rate is 125 bpm.

2. At first observation, there appears to be clear evidence for VA dissociation, with the atrial rate being slower than the ventricular rate. VA “dissociation” is best seen in rhythm leads II and V1.

However, it should be noted that the “dissociated” P waves occur at repeating locations. For complete dissociation, this would require that the VT rate would fortuitously have to be at an exact multiple of the sinus rate.

Furthermore, the P waves are inverted in leads II, III, and aVF, which is not consistent with sinus origin. Therefore, this tracing represents VT with 3:2 VA conduction (VA Wenckebach); this still counts as VA dissociation.

3. Frontal axis is about –90°.

4. The Q wave in aVR is >40 ms, favoring VT.

5. qR in V1 and rS in V6 also favor VT.

Conclusion: VT

Figure 2. A 56-year-old woman with end-stage renal disease presented with dizziness and altered mental status. She has missed her last two hemodialysis appointments.

Figure 2.

An ECG from a 56-year-old woman with end-stage renal disease who presented with dizziness and altered mental status. She had missed her last two hemodialysis appointments.

The ECG in Figure 2 was obtained upon presentation. Her serum potassium was 7.1 mEq/dl, and with aggressive treatment of hyperkalemia, her ECG normalized.

The following observations can be made:

  1. The QRS complexes are wide, measuring about 200 ms; the rate is 125 bpm.

  2. The precordial leads show negative complexes from V1 to V6—so called "negative concordance", favoring VT.

  3. The frontal axis is about +100°.

  4. There are impressively tall, peaked T waves, best seen in lead V3, as expected in hyperkalemia.

  5. The down stroke of the S wave in leads V1 to V3 is swift, <70 ms, favoring SVT with LBBB.

  6. There is a suggestion of a P wave prior to every QRS complex, best seen in lead V1, favoring SVT. As expected, the P waves are of low amplitude in hyperkalemia.

Figure 3. A 70-year-old woman with prior inferior wall MI presented with an episode of syncope resulting in lead laceration, followed by spontaneous recovery by persistent light-headedness. Her initial ECG is shown.

Figure 3.

Initial ECG from a 70-year-old woman with prior inferior wall MI who presented with an episode of syncope resulting in head laceration, followed by spontaneous recovery by persistent light-headedness.

The following observations can be made:

  1. The QRS complex is wide, about 150 ms; the rate is about 190 bpm.

  2. The frontal axis superiorly directed, but otherwise difficult to pin down.

  3. There is precordial (positive) concordance, favoring VT.

  4. Lead aVR shows a broad Q wave, favoring VT.

  5. The QRS complex in lead V1 shows an Rr’ morphology (first rabbit ear is taller than the second), favoring VT (Table IV).

  6. The QRS morphology suggests an old inferior wall myocardial infarction, favoring VT.

Table IV.

ECG findings to help distinguish causes of WCT when the QRS complex in V1 is terminally upright - RBBB-like morphology

Conclusion: VT

Figure 4: A 57-year-old woman with palpitations for many years and idiopathic globally dilated cardiomyopathy was admitted for incessant wide complex tachycardia. The ECG in Figure 4 is representative.

Figure 4.

Representative ECG from a 57-year-old woman with palpitations for many years and idiopathic globally dilated cardiomyopathy was admitted for incessant wide complex tachycardia.

The following observations can be made:

  1. The QRS duration is 170 ms; the rate is 126 bpm.

  2. The frontal axis is about +100°.

  3. The QRS complex in lead V1 shows an rS pattern, with a broad initial R wave, favoring VT (Table V).

  4. The QRS complex down stroke is slurred in aVR, favoring VT.

  5. There appears to be 1:1 association (best seen in leads II and aVR as a deflection on the down slope of the T wave) which, by itself, is not helpful. However, there is subtle but discernible cycle length slowing (marked by the *). When this occurs, the change in R-R interval precedes and predicts the change in P-P interval; in other words, the R-R change drives the P-P change, confirming that this is VT with 1:1 VA conduction.

Table V.

ECG findings to help distinguish causes of WCT when the QRS complex in V1 is terminally negative - LBBB-like morphology

Conclusion: VT with 1:1 VA conduction

Figure 5: An 88-year-old female with a dual-chamber pacemaker presented after three syncopal episodes within 24 hours. Past medical history was significant for type II diabetes, hypertension, hyperlipidemia, and chronic kidney disease (CKD).

Figure 5.

Rhythm strips from an 88-year-old female with a dual-chamber pacemaker who presented after three syncopal episodes within 24 hours. Past medical history was significant for type 2 diabetes, hypertension, hyperlipidemia, and chronic kidney disease. Medications included flecainide 100 mg twice daily (for 5 years) for paroxysmal atrial fibrillation, metoprolol XL 200 mg daily, and aspirin.

Medications included flecainide 100 mg twice daily (for 5 years) for paroxysmal atrial fibrillation, metoprolol XL 200 mg daily, and aspirin. Her rhythm strips from the ambulance are shown in Figure 5.

The following observation can be made:

  1. At first glance (as was the incorrect interpretation by the emergency room physicians), the ECG may be thought to show narrow QRS complexes interspersed with wide QRS complexes. However, the correct interpretation requires recognition that the “narrow complexes” are too narrow to be QRS complexes, and are actually pacemaker spikes with failure to capture the myocardium.

  2. The wide QRS complexes follow some of the pacing spikes, and show varying degrees of QRS widening due to intramyocardial aberrancy. The interval from the pacing spike to the "captured" QRS complex progressively gets longer, before a pacing spike fails to capture altogether; this is consistent with "Pacemaker Exit Wenckebach". The patient was found to have flecainide poisoning with an elevated flecainide level. Once corrected, normal pacing with consistent myocardial capture was noted.

Conclusion: Intermittent loss of pacing capture and aberrancy of intramyocardial conduction due to drug toxicity.

Figure 6: A 65-year-old man with severe alcoholism presented with catastrophic syncope while seated at a bar stool resulting in a cervical spine fracture. His ECG showed LBBB during sinus rhythm (left panel in Figure 6).

Figure 6.

ECG on the left shows LBBB during sinus rhythm in a 65-year-old man with severe alcoholism who presented with catastrophic syncope. ECG on the right shows arrhythmia induced at electrophysiology study.

His echocardiogram showed a severely dilated heart with ejection fraction estimated at 10% to 15%. He proceeded to have an episode of WCT while in bed with dizziness and drop in blood pressure, which self-terminated. He underwent electrophysiology study, where a wide complex tachycardia (right panel in Figure 6) was easily and reproducibly induced with programmed ventricular stimulation.

The following observations can be made:

  1. The QRS duration is 170 ms; the rate is 126 bpm.

  2. The QRS complex during WCT and during sinus rhythm are nearly identical, and show LBBB morphology. These findings would favor SVT.

  3. However, careful observation shows VA dissociation (best seen in lead V1) with slower P waves. This strongly favors VT, especially in the setting of a dilated cardiomyopathy and preexisting LBBB. The intracardiac tracings showed a clear His bundle signal prior to each QRS complex (not shown), confirming the diagnosis of bundle branch reentry. This is one VT which meets every QRS morphology criterion for SVT with aberrancy.

Conclusion: VT due to bundle branch reentry.

Figure 7: The telemetry strip shown in Figure 7 (lead MCL or V1) was recorded in a 42-year-old man with no cardiac history.

Figure 7.

A telemetry strip (lead MCL or V1) recorded in a 42-year-old man with no cardiac history.

The following observations can be made:

  1. The rhythm strip shows sinus tachycardia at the beginning and at the end; each sinus P wave is marked. In between, there is a WCT with a relatively narrow QRS complex with an RBBB-like pattern.

  2. The WCT “overtakes” the sinus P waves starting at the fourth beat, resulting in apparent P–R interval “shortening.” This pattern is pathognomonic of VT, and represents a form of VA dissociation during VT onset.

  3. By the fourth wide complex beat, there is 1:1 VA conduction, and now there is VA association with a retrograde P wave (P’). Note that as the WCT rate oscillates, the retrograde P waves follow the R-R intervals. This is also indicative of VT (ventricular oscillations precede and predict atrial oscillations).

  4. Careful observation of QRS morphology during the WCT shows a qR pattern, also favoring VT. The apparent “narrowness” of the QRS may be misleading in a single lead rhythm strip.

Conclusion: Nonsustained VT

Figure 8: WCT tachycardia recorded in a male patient on postoperative day 3 following mitral valve repair. He had a history of paroxysmal atrial fibrillation.

Figure 8.

ECH showing WCT tachycardia recorded in a male patient on postoperative day 3 following mitral valve repair. He had a history of paroxysmal atrial fibrillation.

The following observations can be made:

  1. The QRS complex is wide, measuring about 130 ms; the frontal axis is rightward and inferior, suggestive of left posterior fascicular block (LPFB).

  2. The QRS complex in rhythm strip V1 shows an RR’ configuration, but with the second rabbit ear taller than the first; this favors SVT with aberrancy.

  3. There are errant pacing spikes (epicardial wires that were undersensing).

Figure 9: After starting intravenous amiodarone, this ECG was obtained.

Figure 9.

ECG in same patient as Figure 8, but after starting intravenous amiodarone.

The following observations can now be made:

  1. The underlying rhythm is now clearly exposed. It is atrial flutter with grouped beating.

  2. The QRS complex is identical to the prior WCT, which was atrial flutter with 2:1 conduction.

  3. Measurement of the two flutter cycle lengths (↔) exactly equals the rate of the WCT in Figure 8.

Conclusion: Atrial flutter with 2:1 AV conduction with preexisting RBBB and LPFB.

Figure 10 and Figure 11: A 62-year-old man without known heart disease but uncontrolled hypertension developed palpitations and light-headedness that prompted him to visit his doctor. A rapid pulse was detected, and the 12-lead ECG shown in Figure 10 was obtained.

Figure 10.

A 12-lead ECG from a 62-year-old man without known heart disease who developed palpitations and light-headedness.

Figure 11.

ECG from same patient as in figure 10, after IV amiodarone was administered.

The following observations can be made from the first ECG:

  1. The WCT shows a QRS complex duration of 180 ms; the rate is 222 bpm.

  2. The frontal axis is pointing to the right shoulder, and favors VT.

  3. There is (negative) precordial concordance, favoring VT.

  4. Leads V2 and V3, however, show swift down strokes (onset to nadir <70 ms), favoring SVT with LBBB aberrancy.

The emergency medical services were summoned and IV amiodarone was administered. The rhythm “broke” and the 12-lead ECG shown in Figure 11 was obtained.

The following observations can be made from the second ECG, obtained after amiodarone:

  1. The heart rate is 111 bpm, with a right inferior axis of about +140° and a narrow QRS.

  2. Although not immediately apparent, the rhythm is now atrial flutter with 2:1 conduction. The flutter waves are marked by arrows (↑).

Conclusion: Atrial flutter with LBBB aberrancy with unusual frontal axis and precordial progression. The exact same pattern of LBBB aberrancy was reproduced during rapid atrial pacing at the time of the electrophysiology study. The rapidity of the S wave down stroke and the exact halving of the ventricular rate after IV amiodarone made the diagnosis of VT suspect, and eventually led to the correct diagnosis of atrial flutter with aberrancy.

Figure 12: A 79-year-old woman with mitral valve stenosis and a dual-chamber pacemaker was admitted with fevers. Her 12-lead ECG, shown in Figure 12, prompted a consultation for evaluation of “nonsustained VT.”

Figure 12.

This 12-lead ECG prompted a consultation for evaluation of “nonsustained VT” in a 79-year-old asymptomatic woman with mitral valve stenosis and a dual-chamber pacemaker.

The following observations can be made:

  1. The ECG shows atrial fibrillation with both narrow and wide QR complexes. All QRS complexes are irregularly irregular.

  2. Although initial perusal may suggest runs of nonsustained VT, careful observation reveals that there is a clear pacing spike prior to each wide QR complex (best seen in lead V4), making the diagnosis of a paced rhythm.

Conclusion: The “nonsustained VT” was actually a paced rhythm due to inappropriate and intermittent tracking of atrial fibrillation by the dual-chamber pacemaker. Once atrial channel was programmed to a more sensitive setting, appropriate “mode-switching” occurred and inappropriate tracking ceased.

Figure 13: A 33-year-old man with lifelong paroxysmal rapid heart action underwent a diagnostic electrophysiology study. The 12-lead rhythm strips shown in Figure 13 were recorded during transition from a WCT to a narrow complex tachycardia.

Figure 13.

The 12-lead rhythm strips were recorded at electrophysiology study during transition from a WCT to a narrow complex tachycardia in a 33-year-old man with paroxysmal palpitations.

The following observations can be made:

  1. The WCT is at a rate of about 100 bpm, has a normal frontal axis, and shows a typical LBBB morphology; the S wave down stroke in V1-V3 is swift (<70 ms). All these findings are consistent with SVT with aberrancy.

  2. Most importantly, the transition to narrow complex tachycardia is accompanied by an acceleration of the heart rate to about 120 bpm. This observation clinches the diagnosis of orthodromic atrioventricular tachycardia using a left-sided accessory pathway (Coumel’s law).

Conclusion: SVT (AVRT utilizing a left-sided accessory pathway) with LBBB aberrancy

What's the Evidence for specific management and treatment recommendations?

Kindwall, KE, Brown, J, Josephson, ME.. "Electrocardiographic criteria for ventricular tachycardia in wide complex left-bundle branch block morphology tachycardias". Am J Cardiol. vol. 15. 1988. pp. 1279-83.

Vereckei, A, Duray, G, Szenasi, G. "Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia". European Heart J. vol. 28. 2007. pp. 589-600.

Brugada, P, Brugada, J, Mont, L. "A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex". Circulation. vol. 83. 1991. pp. 1649-59.

Vereckei, A, Duray, G, Szenasi, G. "New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia". Heart Rhythm. vol. 5. 2008. pp. 89-98.

Goldberger, ZD, Rho, RW, Page, RL.. "Approach to the diagnosis and initial management of the stable adult patient with a wide complex tachycardia". Am J of Cardiol. vol. 101. 2008. pp. 1456-66.

Jastrzebski, M, Kukla, P, Czarnecka, D, Kawecka-Jaszcz, K.. "Comparison of five electrocardiographic methods for differentiation of wide QRS-complex tachycardias". Europace.. vol. 14. 2012 Aug. pp. 1165-71.

Jastrzebski, M, Sasaki, K, Kukla, P, Fijorek, K. "The ventricular tachycardia score: a novel approach to electrocardiographic diagnosis of ventricular tachycardia". Europace.. vol. 18. 2016 Apr. pp. 578-84.

Huemer, M, Meloh, H, Attanasio, P, Wutzler, A. "The Lewis Lead for Detection of Ventriculoatrial Conduction Type". Clin Cardiol. vol. 39. 2016. pp. 126-131.

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