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Ventricular Tachycardia May Masquerade as Supraventricular Tachycardia in Patients With Preexisting Bundle-Branch Block
CASE REPORT
Ventricular Tachycardia May Masquerade as Supraventricular Tachycardia in Patients With Preexisting Bundle-Branch Block From the Department of Internal Medicine, Carolinas Medical Center, Charlotte, North Carolina. Receivedfor publication August 26, 1994. Revision received January 19, 1995. Acceptedfor publicationJanuary 19, 1995. Copyright © by the American College of Emergency Physicians.
Laszlo Littmann,MD Marvin M McCall, MD
We present the cases of three patients with preexisting bundlebranch block in whom wide-complex tachycardias were considered to be of supraventricular origin because QRS morphologies were essentially unchanged from those during normal sinus rhythm. The patients experienced adverse effects from medications for supraventricular tachycardia. Ventricular tachycardia eventually was diagnosed in all three by means of invasive electrophysiologic studies. Ventricular tachycardia may masquerade as supraventricular tachycardia in patients with fixed intraventricular conduction disturbance. Emergencytherapy based solely on the QRS identity criteria may result in poor clinical outcome. [Littmann L, McCall MM: Ventricular tachycardia may masquerade as supraventricular tachycardia in patients with preexisting bundle-branch block: Ann EmergMedJuly1995:26:98-101.] INTRODUCTION Patients presenting with wide-QRS-complex tachycardia may have ventricular tachycardia (VT) or supraventricular tachycardia (SVT) with aberrancy. Despite many publications describing clinical and ECG criteria for differential diagnosis, misidentification (usually in favor of SVT) and inappropriate initial management are common. 1-3 It has been widely held that the differentiation of patients with preexisting bundle-branch block (BBB) is easy: If the QRS complexes during tachycardia are identical to those during sinus rhythm, the tachycardia is supraventricular; if they are different, the arrhythmia is ventricular. 3-5 We present three cases of patients with wide-complex tachycardia whose QRS morphologies were almost identical to those during normal sinus rhythm. The patients, however, exhibited adverse effects from medications aimed at converting SVT. In each patient, electrophysiologic testing eventually disclosed a ventricular origin of the arrhythmia. This rarely appreciated cause of misdiagnosis of VT may occur more commonly than is generally assumed.
98
ANNALS OF EMERGENCY MEDICINE
26:1 JULY
1995
VT & SVT Littmann & McCall
CASE REPORTS
In a 14-month period, we saw three patients with the following clinical, ECG, and electrophysiologic presentations. First, each patient had stable intraventricular conduction disturbance in normal sinus rhythm. Second, they presented with wide-complex tachycardia with a QRS morphology almost identical to that of the QRS complexes during normal sinus rhythm. Third, in two patients medications aimed at converting the SVT were ineffective and were associated with hemodynamic deterioration. Finally, in each case the wide-complex tachycardias were induced subsequently during invasive electrophysiologic testing. His-bundle ECGs revealed the ventricular origin of the arrhythmias. Patient 1 A 59-year-old man with severe ischemic cardiomyopathy and chronic left BBB was admitted to the emergency department for palpitations and shortness of breath. On presentation, he was found to be in widecomplex tachycardia. An ECG during normal sinus rhythm showed left BBB (LBBB), horizontal axis, and both Q waves and S waves in the left lateral leads compatible with a remote myocardial infarction (Figure, A). The QRS duration measured 192 milliseconds. During tachycardia of 176, the QRS morphology was almost identical to that in sinus rhythm (Figure, B). The QRS duration also was unchanged at 196 milliseconds. The tachycardia was presumed to be supraventricular, and the patient received rounds of IV adenosine, diltiazem, and verapamil without success. Verapamil administration was associated with a drop in systemic arterial pressure from 108/86 mm Hg to 64/54 mm Hg. Eventually, because of the negative response to conventional SVT medications, an esophageal electrode was placed, revealing atrioventricular dissociation (Figure, C). A fight ventricular temporary pacemaker electrode was inserted; overdrive pacing of the recurrent tachycardia was successful on several occasions. Electrophysiologic study revealed easily inducible VT with atrioventricular dissociation and no His deflections preceding the QRS complexes. The induced tachycardia morphology was again identical to the supraventricular morphology. The incessant arrhythmia finally was suppressed with a combination of IV procainamide, bretylium, and amiodarone. Patient 2 A 57-year-old man without structural heart disease and normal left ventricular function was admitted with palpitations. The patient had stable right BBB (RBBB) with horizontal frontal plane axis during normal sinus rhythm. The QRS duration on sinus beats measured 128 milliseconds. During tachycardia of 160, the QRS
JULY 1995
26:1
ANNALS OF EMERGENCY MEDICINE
morphology was almost identical to its supraventricular counterpart, with a slightly more pronounced left-axis deviation. The QRS duration measured 136 milliseconds. On the basis of the "supraventricular" pattern of the QRS complexes, the diagnosis of SVT was made. The patient received IV adenosine without effect. Adenosine was followed by IV verapamil, resulting in acceleration of the tachycardia to 178 and a drop in systemic arterial pressure from 118/96 mm Hg to 82/70 mm Hg. Esophageal ECG revealed a 3:2 ventriculoatrial conduction pattern and suggested a ventricular origin of the arrhythmia. The tachycardia eventually was terminated by means of right ventricular overdrive pacing. Electrophysiologic study revealed easily inducible VT with a morphology corresponding to that of the clinical tachycardia. A combination of oral quinidine and propafenone controlled the tachycardia. Patient 3 A 67-year-old man with remote anterior myocardial infarction, left ventricular aneurysm, and severe ischemic cardiomyopathy was admitted with sudden-onset chest pressure and diaphoresis. He was found gure.
VT masquerading as 5VT in patient 1: A, 12-lead ECG during normal sinus rhythm showing LBBB and remote myocardial infarction; B, 12-lead ECG during tachycardia with unchanged QRS morphology compared with A; C, atrioventricular dissociation d~sclosedby esophageal ECG during an episode of spontaneous termination of the tachycardia.*
~
!lI[l
Ii
I Ill
I~.! [ [
Twc-r :v2 ri; :
~~ - ~ P ] ° ~"i~I IavF I ' ~ ' ; iI ' 1 V3,I i I
[
[': ~V 6,
~
jl,~vL::I I J
lye ]
I I 'Vi '1 [ r i [ I~__: : J '_..~_ I_J. ]W_
*11, ECGlead II; Esoph, esophageal recording; P, sinus P wave; A, atrial electrograms. The strips shown in A and B were recorded at a paper speed of 25 rnm/second; C was recorded at 50 rnm/secand.
99
VT & SVT Littmann & McCall
to be in wide-QRS-complex tachycardia. Baseline 12-lead ECG during normal sinus rhythm showed first-degree atrioventricular block, nonspecific intraventricular conduction disturbance, QRS duration of 160 milliseconds, indeterminate frontal plane axis, loss of R waves, and STsegment elevation in the precordial leads. ECG morphology during a tachycardia of 180 was almost identical to the sinus QRS morphology, with some widening of the QRS complex during tachycardia. On the basis of ECG findings and auscuhatory signs of atrioventricular dissociation and our experience with the other two cases, we considered the arrhythmia most likely ventricular in origin. IV lidocaine was ineffective in terminating the tachycardia. IV procainamide slowed it effectively, and the signs of atrioventricular dissociation became more obvious. The patient, however, became hypotensive and had to be cardioverted electrically to normal sinus rhythm. Subsequent serial electrophysiologic studies revealed an easily inducible VT with ECG morphology identical to that in normal sinus rhythm. During tachycardia, atrioventricular dissociation was present and His deflections were absent from the front of ventricular activation. Intracardiac catheter mapping and pace mapping suggested a left ventricular high midseptal origin of the tachycardia. VT became noninducible on therapeutic doses of quinidine and mexiletine. DISCUSSION
Many ECG criteria have been established to distinguish VT from SVT with aberrancy.6,r In patients with preexisting BBB, a QRS morphology during tachycardia identical to that at baseline is generally believed to be a reliable indicator that the arrhythmia is supraventricular. 3-5 Our study shows that VT may masquerade as SVT in patients with fixed intraventricular conduction disturbance. Emergency therapy based solely on the QRS identity criteria may be associated with poor clinical outcome. The occurrence of VT QRS morphology similar or identical to the sinus morphology in patients with preexisting BBB has been described in few case reports. 8-1° Our experience with three additional cases diagnosed during a 14-month period suggests that this scenario is not that uncommon. Patients with fixed LBBB, RBBB, or nonspecific intraventricular conduction disturbance (periinfarction block), with or without structural heart disease, may exhibit VT with a QRS morphology that is practically identical to its counterpart in sinus rhythm. In previously reported casess-l° and in all three of our
10O
cases a one-to-one atrioventricular relationship was absent during the wide-complex tachycardias. Atrioventricular dissociation is exceedingly rare in SVT and for all practical purposes should be considered diagnostic of ventricular origin of aW wide-complex tachycardia.3,6,7 In each of our three cases, in fact, unearthing the dissociated atrial activity led to the proper diagnosis. The exact mechanism whereby supraventricular QRS morphology during VT is maintained in patients with fixed BBB remains speculative. Macroreentry tachycardia involving both bundle branches in the circuit has been described previously 1° but was ruled out in our cases. Another possible mechanism involves a VT site of origin close to the proximal portion of the nonblocked bundle branch# Ectopic impulses rapidly invading the functioning bundle branch would show QRS morphologies identical to those in sinus rhythm. A high left midseptal origin of the VT in patient 3 favors such an explanation. On the basis of the cases described in this and previous reports 8-1°, wide-complex tachycardias should not automatically be considered supraventricular, even if their QRS morphologies are identical to those during sinus rhythm, unless a constant P-QRS relationship can be demonstrated. From a practical perspective, uncertain cases may be identified simply as wide-complex tachycardias and be treated empirically according to current advanced cardiac life support guidelines. 11 In the stable patient, physicians should search for physical and ECG signs of atrioventricular dissociation, using esophageal electrocardiography if necessaW. Once atrioventricular dissociation is documented, the tachycardia should be considered ventricular in origin and treated as such. 11 SUMMARY
In patients with preexisting BBB, the QRS morphology during VT may be similar or identical to that during normal sinus rhythm. Although most patients with fixed BBB who present with apparent SVTs most likely have SVT,3,4 a ventricular origin of the arrhythmia should not be automatically excluded. A diligent search for physical, ECG, and electrophysiologic signs of atrioventricular dissociation (with use of an esophageal electrode, if necessary) should be performed in each case, and the arrhythmia should be considered to have a ventricular origin if atrioventricular dissociation is present. Such an approach would have led to an earlier correct diagnosis and proper management of VT in all three cases in this report.
ANNALS OF EMERGENOY MEBIClNE
26:1
JULY 1995
VT & SVT Littmann & McCall
REFERENCES 1. Dancy M, CaromAJ, Ward D: Misdiagnosia of chronic recurrent ventricular tachycardia. Lancet 1985;2:320-323. 2. Stewart RB, 8ardy GH, Greene HL: Wide complex tachycardia: Misdiagnosis and outcome after emergent therapy. Ann Intern Med 1986;104:766-771. 3. Akhtar M, Shenasa M, Jazayeri M, et ah Wide QRS complex tachycardia: Reappraisalof a common clinical problem. Ann Intern Mad 1988;109:905-912. 4. DongasJ, Lehmann MH, Mahmud R, et ah Value of preexisting bundle branch block in the electrocardiographic differentiation of supraventricular from ventricular origin of wide QRStachycardia. Am J Cardiel 1985;55:717-721. 5. Kremers MS, Black WH, Wells PJ, et ah Effect of preexisting bundle branch block on the electrocardiographic diagnosis of ventricular tachycardia. Am J Cardiot 1988;62:1208-1212. 6. Wellens HJJ, B~r FWHM, Lie Kh The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am J Mad 1978;64:27-33. 7. Brugada P, BrugadaJ, Mont L, et ah A new approachto the differential diagnosis of a regular tachycardia with a wide QRS complex. Circa/arian 1991;83:1649-1659.
The authors thank Dr Norris B Harbold, Jr; Dr Alan M Thomley, and Dr Robert M Bersin from the Sanger Clinic, Private Association (Charlotte, North Carolina), for allowing use of the clinical, ECG, and electrophysiologic data of their patients.
Reprint no. 47/1/65121 Address for reprints: Laszlo Littmann, MD Department of Internal Medicine Carolinas Medical Center PO Box 32861 Charlotte, North Carolina 28232 704-355-3165 Fax 704-355-7626
8. Ross DL, Vohra JK, SIomanJG: Similar QRS morphology in sinus rhythm and ventricular tachycardia. PACEPacing C/in Electrophysiol 1979;2:486-489. 9. OlshanskyB: Ventricular tachycardia masqueradingas supraventricurartachycardia: A wolf in a sheep's clothing. J Electrocardio11988;21:377-384. 10. Wang PJ, Friedman PL: "Clockwise" and "counterclockwise" bundle branch reentry as a mechanism for sustained ventricular tachycardfa masqueradingas supraventricular tachycardia. PACEPacing Clin Electrephysiol1989;12:1426-1432. 11. EmergencyCardiac Care Committee and Subcommittees,American Heart Association: Guidelines for cardiopulmonary resuscitation and emergencycardiac care. Ill. Adult advanced cardiac life support. JAMA 1992;268:2199-2241.
JULY 1995 26:1
ANNALS OF EMERGENCY MEDICINE
101
Ventricular Tachycardia May Masquerade as Supraventricular Tachycardia in Patients With Preexisting Bundle-Branch Block From the Department of Internal Medicine, Carolinas Medical Center, Charlotte, North Carolina. Receivedfor publication August 26, 1994. Revision received January 19, 1995. Acceptedfor publicationJanuary 19, 1995. Copyright © by the American College of Emergency Physicians.
Laszlo Littmann,MD Marvin M McCall, MD
We present the cases of three patients with preexisting bundlebranch block in whom wide-complex tachycardias were considered to be of supraventricular origin because QRS morphologies were essentially unchanged from those during normal sinus rhythm. The patients experienced adverse effects from medications for supraventricular tachycardia. Ventricular tachycardia eventually was diagnosed in all three by means of invasive electrophysiologic studies. Ventricular tachycardia may masquerade as supraventricular tachycardia in patients with fixed intraventricular conduction disturbance. Emergencytherapy based solely on the QRS identity criteria may result in poor clinical outcome. [Littmann L, McCall MM: Ventricular tachycardia may masquerade as supraventricular tachycardia in patients with preexisting bundle-branch block: Ann EmergMedJuly1995:26:98-101.] INTRODUCTION Patients presenting with wide-QRS-complex tachycardia may have ventricular tachycardia (VT) or supraventricular tachycardia (SVT) with aberrancy. Despite many publications describing clinical and ECG criteria for differential diagnosis, misidentification (usually in favor of SVT) and inappropriate initial management are common. 1-3 It has been widely held that the differentiation of patients with preexisting bundle-branch block (BBB) is easy: If the QRS complexes during tachycardia are identical to those during sinus rhythm, the tachycardia is supraventricular; if they are different, the arrhythmia is ventricular. 3-5 We present three cases of patients with wide-complex tachycardia whose QRS morphologies were almost identical to those during normal sinus rhythm. The patients, however, exhibited adverse effects from medications aimed at converting SVT. In each patient, electrophysiologic testing eventually disclosed a ventricular origin of the arrhythmia. This rarely appreciated cause of misdiagnosis of VT may occur more commonly than is generally assumed.
98
ANNALS OF EMERGENCY MEDICINE
26:1 JULY
1995
VT & SVT Littmann & McCall
CASE REPORTS
In a 14-month period, we saw three patients with the following clinical, ECG, and electrophysiologic presentations. First, each patient had stable intraventricular conduction disturbance in normal sinus rhythm. Second, they presented with wide-complex tachycardia with a QRS morphology almost identical to that of the QRS complexes during normal sinus rhythm. Third, in two patients medications aimed at converting the SVT were ineffective and were associated with hemodynamic deterioration. Finally, in each case the wide-complex tachycardias were induced subsequently during invasive electrophysiologic testing. His-bundle ECGs revealed the ventricular origin of the arrhythmias. Patient 1 A 59-year-old man with severe ischemic cardiomyopathy and chronic left BBB was admitted to the emergency department for palpitations and shortness of breath. On presentation, he was found to be in widecomplex tachycardia. An ECG during normal sinus rhythm showed left BBB (LBBB), horizontal axis, and both Q waves and S waves in the left lateral leads compatible with a remote myocardial infarction (Figure, A). The QRS duration measured 192 milliseconds. During tachycardia of 176, the QRS morphology was almost identical to that in sinus rhythm (Figure, B). The QRS duration also was unchanged at 196 milliseconds. The tachycardia was presumed to be supraventricular, and the patient received rounds of IV adenosine, diltiazem, and verapamil without success. Verapamil administration was associated with a drop in systemic arterial pressure from 108/86 mm Hg to 64/54 mm Hg. Eventually, because of the negative response to conventional SVT medications, an esophageal electrode was placed, revealing atrioventricular dissociation (Figure, C). A fight ventricular temporary pacemaker electrode was inserted; overdrive pacing of the recurrent tachycardia was successful on several occasions. Electrophysiologic study revealed easily inducible VT with atrioventricular dissociation and no His deflections preceding the QRS complexes. The induced tachycardia morphology was again identical to the supraventricular morphology. The incessant arrhythmia finally was suppressed with a combination of IV procainamide, bretylium, and amiodarone. Patient 2 A 57-year-old man without structural heart disease and normal left ventricular function was admitted with palpitations. The patient had stable right BBB (RBBB) with horizontal frontal plane axis during normal sinus rhythm. The QRS duration on sinus beats measured 128 milliseconds. During tachycardia of 160, the QRS
JULY 1995
26:1
ANNALS OF EMERGENCY MEDICINE
morphology was almost identical to its supraventricular counterpart, with a slightly more pronounced left-axis deviation. The QRS duration measured 136 milliseconds. On the basis of the "supraventricular" pattern of the QRS complexes, the diagnosis of SVT was made. The patient received IV adenosine without effect. Adenosine was followed by IV verapamil, resulting in acceleration of the tachycardia to 178 and a drop in systemic arterial pressure from 118/96 mm Hg to 82/70 mm Hg. Esophageal ECG revealed a 3:2 ventriculoatrial conduction pattern and suggested a ventricular origin of the arrhythmia. The tachycardia eventually was terminated by means of right ventricular overdrive pacing. Electrophysiologic study revealed easily inducible VT with a morphology corresponding to that of the clinical tachycardia. A combination of oral quinidine and propafenone controlled the tachycardia. Patient 3 A 67-year-old man with remote anterior myocardial infarction, left ventricular aneurysm, and severe ischemic cardiomyopathy was admitted with sudden-onset chest pressure and diaphoresis. He was found gure.
VT masquerading as 5VT in patient 1: A, 12-lead ECG during normal sinus rhythm showing LBBB and remote myocardial infarction; B, 12-lead ECG during tachycardia with unchanged QRS morphology compared with A; C, atrioventricular dissociation d~sclosedby esophageal ECG during an episode of spontaneous termination of the tachycardia.*
~
!lI[l
Ii
I Ill
I~.! [ [
Twc-r :v2 ri; :
~~ - ~ P ] ° ~"i~I IavF I ' ~ ' ; iI ' 1 V3,I i I
[
[': ~V 6,
~
jl,~vL::I I J
lye ]
I I 'Vi '1 [ r i [ I~__: : J '_..~_ I_J. ]W_
*11, ECGlead II; Esoph, esophageal recording; P, sinus P wave; A, atrial electrograms. The strips shown in A and B were recorded at a paper speed of 25 rnm/second; C was recorded at 50 rnm/secand.
99
VT & SVT Littmann & McCall
to be in wide-QRS-complex tachycardia. Baseline 12-lead ECG during normal sinus rhythm showed first-degree atrioventricular block, nonspecific intraventricular conduction disturbance, QRS duration of 160 milliseconds, indeterminate frontal plane axis, loss of R waves, and STsegment elevation in the precordial leads. ECG morphology during a tachycardia of 180 was almost identical to the sinus QRS morphology, with some widening of the QRS complex during tachycardia. On the basis of ECG findings and auscuhatory signs of atrioventricular dissociation and our experience with the other two cases, we considered the arrhythmia most likely ventricular in origin. IV lidocaine was ineffective in terminating the tachycardia. IV procainamide slowed it effectively, and the signs of atrioventricular dissociation became more obvious. The patient, however, became hypotensive and had to be cardioverted electrically to normal sinus rhythm. Subsequent serial electrophysiologic studies revealed an easily inducible VT with ECG morphology identical to that in normal sinus rhythm. During tachycardia, atrioventricular dissociation was present and His deflections were absent from the front of ventricular activation. Intracardiac catheter mapping and pace mapping suggested a left ventricular high midseptal origin of the tachycardia. VT became noninducible on therapeutic doses of quinidine and mexiletine. DISCUSSION
Many ECG criteria have been established to distinguish VT from SVT with aberrancy.6,r In patients with preexisting BBB, a QRS morphology during tachycardia identical to that at baseline is generally believed to be a reliable indicator that the arrhythmia is supraventricular. 3-5 Our study shows that VT may masquerade as SVT in patients with fixed intraventricular conduction disturbance. Emergency therapy based solely on the QRS identity criteria may be associated with poor clinical outcome. The occurrence of VT QRS morphology similar or identical to the sinus morphology in patients with preexisting BBB has been described in few case reports. 8-1° Our experience with three additional cases diagnosed during a 14-month period suggests that this scenario is not that uncommon. Patients with fixed LBBB, RBBB, or nonspecific intraventricular conduction disturbance (periinfarction block), with or without structural heart disease, may exhibit VT with a QRS morphology that is practically identical to its counterpart in sinus rhythm. In previously reported casess-l° and in all three of our
10O
cases a one-to-one atrioventricular relationship was absent during the wide-complex tachycardias. Atrioventricular dissociation is exceedingly rare in SVT and for all practical purposes should be considered diagnostic of ventricular origin of aW wide-complex tachycardia.3,6,7 In each of our three cases, in fact, unearthing the dissociated atrial activity led to the proper diagnosis. The exact mechanism whereby supraventricular QRS morphology during VT is maintained in patients with fixed BBB remains speculative. Macroreentry tachycardia involving both bundle branches in the circuit has been described previously 1° but was ruled out in our cases. Another possible mechanism involves a VT site of origin close to the proximal portion of the nonblocked bundle branch# Ectopic impulses rapidly invading the functioning bundle branch would show QRS morphologies identical to those in sinus rhythm. A high left midseptal origin of the VT in patient 3 favors such an explanation. On the basis of the cases described in this and previous reports 8-1°, wide-complex tachycardias should not automatically be considered supraventricular, even if their QRS morphologies are identical to those during sinus rhythm, unless a constant P-QRS relationship can be demonstrated. From a practical perspective, uncertain cases may be identified simply as wide-complex tachycardias and be treated empirically according to current advanced cardiac life support guidelines. 11 In the stable patient, physicians should search for physical and ECG signs of atrioventricular dissociation, using esophageal electrocardiography if necessaW. Once atrioventricular dissociation is documented, the tachycardia should be considered ventricular in origin and treated as such. 11 SUMMARY
In patients with preexisting BBB, the QRS morphology during VT may be similar or identical to that during normal sinus rhythm. Although most patients with fixed BBB who present with apparent SVTs most likely have SVT,3,4 a ventricular origin of the arrhythmia should not be automatically excluded. A diligent search for physical, ECG, and electrophysiologic signs of atrioventricular dissociation (with use of an esophageal electrode, if necessary) should be performed in each case, and the arrhythmia should be considered to have a ventricular origin if atrioventricular dissociation is present. Such an approach would have led to an earlier correct diagnosis and proper management of VT in all three cases in this report.
ANNALS OF EMERGENOY MEBIClNE
26:1
JULY 1995
VT & SVT Littmann & McCall
REFERENCES 1. Dancy M, CaromAJ, Ward D: Misdiagnosia of chronic recurrent ventricular tachycardia. Lancet 1985;2:320-323. 2. Stewart RB, 8ardy GH, Greene HL: Wide complex tachycardia: Misdiagnosis and outcome after emergent therapy. Ann Intern Med 1986;104:766-771. 3. Akhtar M, Shenasa M, Jazayeri M, et ah Wide QRS complex tachycardia: Reappraisalof a common clinical problem. Ann Intern Mad 1988;109:905-912. 4. DongasJ, Lehmann MH, Mahmud R, et ah Value of preexisting bundle branch block in the electrocardiographic differentiation of supraventricular from ventricular origin of wide QRStachycardia. Am J Cardiel 1985;55:717-721. 5. Kremers MS, Black WH, Wells PJ, et ah Effect of preexisting bundle branch block on the electrocardiographic diagnosis of ventricular tachycardia. Am J Cardiot 1988;62:1208-1212. 6. Wellens HJJ, B~r FWHM, Lie Kh The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am J Mad 1978;64:27-33. 7. Brugada P, BrugadaJ, Mont L, et ah A new approachto the differential diagnosis of a regular tachycardia with a wide QRS complex. Circa/arian 1991;83:1649-1659.
The authors thank Dr Norris B Harbold, Jr; Dr Alan M Thomley, and Dr Robert M Bersin from the Sanger Clinic, Private Association (Charlotte, North Carolina), for allowing use of the clinical, ECG, and electrophysiologic data of their patients.
Reprint no. 47/1/65121 Address for reprints: Laszlo Littmann, MD Department of Internal Medicine Carolinas Medical Center PO Box 32861 Charlotte, North Carolina 28232 704-355-3165 Fax 704-355-7626
8. Ross DL, Vohra JK, SIomanJG: Similar QRS morphology in sinus rhythm and ventricular tachycardia. PACEPacing C/in Electrophysiol 1979;2:486-489. 9. OlshanskyB: Ventricular tachycardia masqueradingas supraventricurartachycardia: A wolf in a sheep's clothing. J Electrocardio11988;21:377-384. 10. Wang PJ, Friedman PL: "Clockwise" and "counterclockwise" bundle branch reentry as a mechanism for sustained ventricular tachycardfa masqueradingas supraventricular tachycardia. PACEPacing Clin Electrephysiol1989;12:1426-1432. 11. EmergencyCardiac Care Committee and Subcommittees,American Heart Association: Guidelines for cardiopulmonary resuscitation and emergencycardiac care. Ill. Adult advanced cardiac life support. JAMA 1992;268:2199-2241.
JULY 1995 26:1
ANNALS OF EMERGENCY MEDICINE
101