Electrocardiographic manifestations: aberrant ventricular conduction1

The Journal of Emergency Medicine, Vol. 19, No. 4, pp. 363–367, 2000 Copyright © 2000 Elsevier Science Inc. Printed in the USA. All rights reserved 0736-4679/00 $–see front matter

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Selected Topics: Cardiology Commentary

ELECTROCARDIOGRAPHIC MANIFESTATIONS: ABERRANT VENTRICULAR CONDUCTION Marc L. Pollack,

MD, PhD,*

Theodore C. Chan,

MD,†

and William J. Brady,

MD‡

*Department of Emergency Medicine, York Hospital, York, Pennsylvania; †Department of Emergency Medicine, University of California San Diego Medical Center, San Diego, California; and ‡Department of Emergency Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia Reprint Address: Marc Pollack, MD, PhD, Department of Emergency Medicine, York Hospital, York, PA 17405

e Abstract—Aberrant ventricular conduction is a common electrocardiographic (EKG) manifestation that occurs when the supraventricular electrical impulse is conducted abnormally through the ventricular conducting system. This results in a wide QRS complex that may be confused with a ventricular ectopic beat. This differentiation is important because the treatment and prognosis is quite different. Hemodynamically unstable patients with a widecomplex tachycardia should be promptly cardioverted. Although up to 10% of cases will defy differentiation, ventricular tachycardia and aberrant conduction can be distinguished utilizing history, physical examination, and EKG criteria. The mechanisms of aberrant ventricular conduction are discussed. © 2000 Elsevier Science Inc.

the ventricle is ventricular tachycardia. The non-ventricular wide-complex tachycardias, which originate proximal to the ventricles, may be from a pre-existing bundlebranch block (BBB), antegrade conduction down an accessory pathway, or transient aberrant conduction. This dichotomy of etiologies, ventricular or supraventricular, reflect very different prognostic implications and treatment modalities. The electrocardiographic (EKG) appearances are similar, but treating ventricular tachycardia (VT) as supraventricular tachycardia with aberrancy (SVTA) with calcium channel blocking agents may result in serious morbidity and mortality (2– 4). Furthermore, a dysrhythmia can be of ventricular origin and yet be benign, such as in fasicular tachycardia (5).

e Keywords—aberrant conduction; ventricular tachycardia; electrocardiogram; dysrhythmia

CASE PRESENTATIONS INTRODUCTION

Case 1

In a patient who has a wide-complex tachycardia, the Emergency Physician (EP) must rapidly determine the origin of the wide complexes and initiate appropriate treatment (1). These patients may be hemodynamically unstable so decisions must be made quickly. A widecomplex tachycardia can be of ventricular origin or of atrial origin with abnormal, or aberrant, conduction. A wide-complex tachycardia that has its origin within

A 49-year-old woman came to the Emergency Department (ED) with a chief complaint of “my heart is racing.” She had mild mid-sternal chest pressure, but no shortness of breath or dizziness. There was a past history of hypertension treated with atenolol. She had a history of cigarette smoking and caffeine intake (5 cups of coffee/day), but no history of alcohol or cocaine use. Examination revealed a rapid irregularly irregular heart

Selected Topics: Cardiology Commentary is coordinated by Theodore C. Chan, MD, of the University of California San Diego Medical Center, San Diego, California

RECEIVED: 12 June 2000; ACCEPTED: 21 June 2000 363

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Figure 1. Rapid atrial fibrillation. Five beats of a wide-complex tachycardia that begins after a long R-R interval. This demonstrates aberrant ventricular conduction or Ashman’s Phenomenon.

beat, clear lungs, a blood pressure (BP) of 100/60 mm Hg and pulse rate of 80 to 120 beats/min (bpm). The 12-lead electrocardiogram (EKG) showed no ischemia or injury. The rhythm strip in Figure 1 shows atrial fibrillation with a rapid ventricular response of about 220 bpm and a narrow QRS complex. There is a run of a widecomplex, irregular tachycardia. These aberrantly conducted beats are preceded by a longer than usual R-R interval.

Case 2 A 53-year-old man presented to the ED with palpitations for 1 h. He had no associated chest pain, dizziness, or syncope. He had been recently discharged after an uncomplicated anterior-wall myocardial infarction (MI) followed by stenting of the left-anterior descending artery. A three-lead rhythm strip (Figure 2) showed RBBB aberration caused by retrograde concealed conduction following a left ventricular PVC. This rhythm was subsequently terminated by another left ventricular premature ventricular contractions (PVC).

Electrophysiology Sir Thomas Lewis coined the term “aberrant beats” in 1910 in reference to “impulses that have gone astray.” (6) He believed that bundle branch block was a form of permanent ventricular aberration. We now think of aberrant conduction as transient abnormal conduction through the ventricle—an impulse that begins in the sinus node or elsewhere in the atrium, which is conducted normally through the A-V (atrio-ventricular) junction, but conducted abnormally (aberrantly) in the ventricular conducting system. This is in contrast to PVC that have their origin in the ventricles. The basic cause of aberrant conduction is the premature arrival of a stimulus before the conduction system has completely recovered from its refractory state from the previous beat. The factors that influence refractoriness are rate and preceding cycle length. Several electrophysiologic mechanisms may be responsible for aberrant ventricular conduction. First, stimulation during phase 3 of the action potential can result in aberration. When the stimulus reaches the right bundle branch (RBB) during phase 3, the membrane potential is

Figure 2. RBBB aberration caused by retrograde concealed conduction following a left ventricular ectopic complex. A second ventricular complex breaks the pattern.

Aberrant Ventricular Conduction

reduced and conduction is compromised, particularly if the refractory period is abnormally prolonged and the stimulated rate rapid. This phenomenon is often called tachycardia-dependent BBB. Second, aberrant conduction can result from retrograde concealed conduction (as seen in Case 2). Such retrograde concealed conduction occurs when a VPB activates the RBB in a retrograde manner. As activation occurs late, the RBB is subsequently in the refractory period for the next sinus beat, resulting in aberrant conduction through the ventricle. The RBB is again activated in a retrograde manner, leaving it refractory once again to the next sinus beat. This delayed retrograde activation continues until another VPB breaks the cycle (Figure 2). Third, another etiology of aberrancy occurs when the RBB action potential does not reach threshold potential (phase 4 aberration). This rare phenomenon can occur in the setting of bradycardia.

365 Table 1. Origin of Wide-QRS-Complex Tachycardia [Adapted from (9)] Criteria QRS ⬎ 0.16s QRS ⬎ 0.14s AV Dissociation V1-RBBB morphology with large left peak V6-RBBB morphology with rS Precordial Concordance

Favors Sensitivity Specificity VT VT VT

65% 79% 24%

97% 69% 100%

VT VT VT

23% 38% 9%

100% 100% 100%

chrony results in intermittent atrial contraction against a closed tricuspid valve (10), resulting in large amplitude, irregular jugular venous pulsations. In addition, AV asynchrony results in variability of cardiac output and differences in the intensity of the heart sounds, especially the first heart sound (S1).

ELECTROCARDIOGRAPHIC DIAGNOSIS APPROACH TO THE PATIENT WITH WIDE-COMPLEX TACHYCARDIA The first step in evaluating the patient with a widecomplex tachycardia is to determine if the dysrhythmia must be promptly terminated. This decision is not based on rhythm diagnosis but on hemodynamic stability. If the tachycardia is associated with cardiac ischemia, hypotension, syncope, or end-organ hypoperfusion, prompt cardioversion is indicated. Hemodynamic stability during the tachycardia, however, is not a good criterion to use to determine the etiology of the dysrhythmia (7). Signs and symptoms associated with a tachycardia are due to the elevated heart rate, associated heart disease, and left ventricular function rather than the etiology of the tachycardia (8). If the tachycardia is well tolerated hemodynamically, taking the time to determine the origin of the dysrhythmia is appropriate. Initial evaluation should include history of the present illness, past history, current medications, physical examination, a 12-lead EKG, serum potassium level and, if possible, a prior EKG. A single lead rhythm strip is inadequate and frequently results in misdiagnosis and consequent mismanagement (9). A history of coronary heart disease, MI, or congestive heart failure strongly suggests VT, not aberrant conduction (10). The objective of physical examination in this situation is to determine if there is evidence of AV dissociation. Although AV dissociation is common in VT, it is detectable on physical examination in only a minority of patients (7). Cannon A waves may be seen on jugular venous examination. They occur because AV asyn-

Many investigators have attempted to define electrocardiographic criteria by which to separate VT from SVTA (1,7,10 –12). The results of these studies, despite their clinical usefulness, are limited due to the lack of a “gold” or criterion standard by which to define the dysrhythmia. Differentiating VT from SVTA by 12-lead EKG can be very difficult. One study, for example, shows 22% disagreement among Emergency Physicians using the Brugada criteria (11,13) Drew and Scheinman evaluated EKG criteria for VT and SVTA using intracardiac electrophysiologic mapping as the criterion standard (9). Because they used a true “gold standard” for defining the dysrhythmia, their results are worth reviewing in some detail (summarized in Table 1). On clinical presentation, those with SVTA are younger and have better LV function. They are less likely to have a past history of myocardial infarction. Although the average heart rate is 190 bpm for both the SVTA and VT groups, Drew and Scheinman demonstrate that the 12-lead EKG, unlike the rhythm strip, can differentiate VT from SVTA in the large majority of patients. In fact, only 10% of wide-complex tachycardias defy differentiation of VT from SVTA. Difficulty is encountered in those with heart rates over 190 bpm (9). In terms of EKG findings, whereas only 19% of the VT group demonstrate AV dissociation, this finding is 100% specific for VT. AV dissociation is more easily detected in those with slower heart rates and the dissociated P waves are most commonly seen in lead V1. Sixty-five percent of the VT patients have a QRS complex wider than 0.16 (with a specificity of 97%). This

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Figure 3. Lead V1 showing a RBBB configuration where the left peak is larger than the right. This finding is specific for a ventricular origin of the complex.

criterion, however, is less useful in those with rapid rates (⬎190 bpm). Precordial QRS concordance is seen in only 9% of VT patients, but is 100% specific for VT. Though uncommon, a fusion or capture beat is also highly specific for VT. Drew and Scheinman report that RBBB morphology in lead V1 is seen in 82% of VT patients (9). In their study, the finding of a taller left notch of the RBBB is 100% specific for VT (Figure 3). However, aberrancy also usually appears as a RBBB pattern. Wellens, Bar, and Lie report that 69% of cases are RBBB in configuration, whereas Sandler and Marriott report the incidence to be even higher at 80 – 85% (4,14). Most likely, this finding is the result of the fact that the RBB is longer, conducts more slowly, and as a result, has a longer refractory period than the LBB (15). When cycle length varies widely from beat to beat, such as in atrial fibrillation, aberrancy is commonly observed (as seen in Case 1). This particular type of ventricular aberrancy was first described in 1947 by Gouaux and Ashman and is commonly referred to as Ashman’s Phenomenon (16). The refractory period of the bundle branches, and in particular the right, is increased and likely to be greater than that of the AV node (17–19). Other sources of early beats such as premature atrial contractions (PACs) and nodal beats will conduct aberrantly if they reach the ventricle during the refractory period. Rate-dependent BBB is a type of aberrant conduction that intermittently appears as the heart rate changes. The critical heart rate for development of aberration is often faster than the rate for disappearance as a result of differing refractory periods for slower and faster heart rates (20). For children, although VT is uncommon, SVTA is an even rarer occurrence (21). In one series, only 10 of 120 children with SVT (8%) had a wide QRS complex during tachycardia (22). In addition, no patient with a normal QRS in normal sinus rhythm had a prolonged QRS during episodes of SVT. If a child has a tachycardia with

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a widened QRS complex, the chances are greater than 90% that the wide complex is of ventricular origin. Finally, in a patient with wide-complex tachycardia, other potential etiologies besides VT and SVTA must be considered. Chief among these is an accessory pathway, such as in the Wolf-Parkinson-White Syndrome (WPW). The WPW can be differentiated from aberrantly conducted beats by the presence of a delta wave and a shortened PR interval. Another common cause is the pre-existing BBB that can mimic VT or SVTA. In fact, VT may appear with a wide QRS morphology that is identical to that of its morphology when in a sinus rhythm (23,24). Additional causes of wide complexes include hyperkalemia, anticholinergic medications, and a variety of other drugs (25). There are also other dysrhythmias of ventricular origin, such as fasicular tachycardia, that can mimic VT and SVTA (5). Conversely, on occasion VT may present with a narrow QRS complex (26). Finally, artifact may also mimic VT (27).

CONCLUSION Patients with a wide-complex tachycardia should be immediately cardioverted if hemodynamically compromised. If stable, time should be taken to accurately determine the rhythm. The history, physical examination, and 12-lead EKG should be utilized to differentiate VT from SVTA. Despite all efforts, 10% will defy determination and should be treated as VT until proven otherwise. Other causes of wide-complex tachycardia, such as effect of medications, hyperkalemia, and WPW also should be considered.

REFERENCES 1. Brady WJ, Skiles J. Wide QRS complex TACHYCARDIA: ECG differential diagnosis. Am J Emerg Med 1999;17:376 – 81. 2. Stewart RB, Bardy GH, Greene HL. Wide complex tachycardia: misdiagnosis and outcome after emergent therapy. Ann Int Med 1986;104:766 –71. 3. Buxton AE, Marchlinski FE, Doherty JU, et al. Hazards of intravenous verapamil for sustained ventricular tachycardia. Am J Cardiol 1987;57:1107. 4. Akhtar M, Tchou P, Jazayeri M. Use of calcium channel-entry blockers in the treatment of cardiac arrhythmias. Circulation 1989; 80:IV31. 5. Elswick BD, Niemann JT. Fasicular ventricular tachycardia: an uncommon but distinctive form of ventricular tachycardia. Ann Emerg Med 1998;31:406 –9. 6. Lewis T. Paroxysmal tachycardia, the result of ectopic impulse formation. Heart 1910;1:262. 7. Marriott HJ. Differential diagnosis of supraventricular and ventricular tachycardia. Cardiology 1990;77:209 –20. 8. Akhtar M, Shenasa M, Jazayeri M, et al. Wide QRS complex tachycardia: reappraisal of a common clinical problem. Ann Intern Med 1988;109:905–12.

Aberrant Ventricular Conduction 9. Drew BJ, Scheinman MM. ECG criteria to distinguish between aberrantly conducted supraventricular tachycardia and ventricular tachycardia. Pacing Clin Electrophysiol 1995;18:2194 –208. 10. Shah P, Thakur RK, Xie B, Hoon VK. clinical approach to wide QRS complex tachycardias. Emerg Med Clin N Am 1998;16:331– 60. 11. Brugada P, Brugada J, Mont L, et al. A new approach to the differential diagnosis of regular tachycardia with a wide QRS complex. Circulation 1991;83:1649 –59. 12. Levitt MA. Supraventricular tachycardia with aberrant conduction versus ventricular tachycardia. Differentiation and diagnosis. Am J Emerg Med 1988;6:273–7. 13. Herbert ME, Votey SR, Morgan MT, et al. Failure to agree on ECG diagnosis of ventricular tachycardia. Ann Emerg Med 1996;27: 35– 8. 14. Wellens HJJ, Bar FWHM, Lie KI. The VALUE of the EKG in the differential diagnosis of a tachycardia with a widened QRS complex. Am J Med 1978;64:27. 15. Moe GK, Mendez C, Han J. Aberrant AV impulse propagation in the dog heart: A study of functional bundle-branch block. Circ Res 1965;16:261. 16. Gouaux JL, Ashman R. Auricular fibrillation with aberration simulating ventricular paroxysmal tachycardia. Am Heart J 1947;34: 366. 17. Suyama AC, Sunagawa K, Sugimachi M, et al. Differentiation between aberrant ventricular conduction and ventricular ectopy in atrial fibrillation using RR interval Scattergram. Circulation 1993; 88:2307. 18. Chenevert M, Lewis RJ. Ashman’s phenomenon—a source of

367

19.

20. 21.

22.

23.

24.

25.

26. 27.

non-sustained wide-complex tachycardia: case report and discussion. J Emerg Med 1992;10:174. Denker ST, Gilbert CJ, Shenasa M, et al. An electrocardiographic– electrophysiologic correlation of aberrant ventricular conduction in man. J Electrocardiol 1983;16:269. Marriott HJL, Conover MB. Advanced concepts in arrhythmias, third edition. St. Louis: Mosby; 1998. Meldon SW, Brady WJ, Berger S, Mannenbach M. Pediatric ventricular tachycardia: a review with three illustrative cases. Pediatr Emerg Care 1994;10:294 –300. Garson A. Ventricular arrhythmias. In: Gillette P, Barson A, eds. Pediatric arrhythmias: electrophysiology and pacing. Philadelphia: WB Saunders; 1990:440. Oreto G, Smeets JLRM, Rodriguez L, et al. Wide complex tachycardia with atrioventricular dissociation on qrs morphology identical to that of sinus rhythm: a manifestation of bundle branch reentry. Heart 1996;76:541–7. Littmann L, McCall MM. Ventricular tachycardia may masquerade as supraventricular tachycardia in patients with preexisting bundle branch block. Ann Emerg Med 1995;26:98 –101. Richter J, Burbach G, Hellgren V, et al. Aberrant atrioventricular conduction triggered by antimalarial prophylaxis with mefloquine. Lancet 1997;349:101–2. Hayes JJ, Stewart RB, Greene HL, et al. Narrow QRS ventricular tachycardia. Ann Int Med 1991;114:460 –3. Knight BP, Pelosi F, Michard GF, et al. Clinical consequences of electrocardiographic artifact mimicking ventricular tachycardia. N Engl J Med 1999;341:1270.