Many papers have been written (and careers made) analyzing QRS morphology as a clue to the origin of a wide-complex tachycardia (WCT). The original one was the classic study of Wellens (1) who popularized the morphologic criteria in leads V1 and V6. In general, as you might expect, highly specific criteria have a low sensitivity. Examples of the latter include the presence of AV dissociation, bizarre axis (-90 to -270), the presence of capture or fusion beats, the presence of a _positive_ conconcordance across the precordium (100% specific or very close to it), the presence of LBBB with RAD, a QRS width of greater than 140 ms with RBBB or greater than 160 ms with LBBB (highly suggestive unless the patient is on class Ic drugs). Utilizing these criteria a corrct diagnosis could not be made in 8% of patients with VT and 14% of patients with SVT would have been incorrectly labeled as VT (2).Prompted by the lack of both highly sensitive and specific ECG criteria other authors have attempted to elaborate on these observations. Kindwall(3) using the following 4 criteria to have a high predictive accuracy: 1) a R wave in V1 or V2 greater than 30 ms 2) any Q wave in V6 3) a greater than 60 ms duration from the onset of the QRS to the nadir of the S wave in V1 or V2 and 4) notching of the downstroke of the S wave in V1 or V2. Prompted by the results of this study Brugada et. al. (4) hypothesized that measuring the interval from the onset of the R wave to the nadir of the S wave in _any_precordial lead would be diagnostic of the presence of VT. After analying 554 WCT they proposed the following 4-step algorithm 1) if NO RS complex is present in any precorial lead then the diagnosis is VT...failing that 2) if _any_ RS interval (onset of R to nadir of S) is greater than 100ms then the diagnosis is VT..failing that 3) if AV dissociation is present then the diagnosis is VT....failing that 4) if specific morphologic criteria were present in V1 and V6 the diagnosis is VT. A negative answer to the last four questions implies the presence of abberant conduction. They found a sensitivity of 0.987 and specificity of 0.965 with this method. Consider that in the presence of WCT VT is much more likely than SVT by a factor of 3:1 in most studies. Certain historical features, such as the history of an MI, CHF, angina or age greater than 35, can increase this ratio considerably (5). Physicians long ago relinquished the idea that a patient with WCT who was hemodynamically stable would have to have SVT with aberrency. In this particular case you mention the presence of concordance during the WCT. Was it positive or negative? If the answer is the former then the diagnosis is VT. If the latter, than VT is still much more likely but about 14% of SVT will have this finding (6). The presence of LAD makes VT more likely but not by a definitive margin. There is a large overlap in rates of SVT and VT so a rate of 120 is not very helpful in distinguishing between the two . A QRS width of 140 ms does not rule out VT as 15% of these patients will have complexes narrower than this (2). I wonder about the significance of the fact that you occasionally observed rates of 120 with narrow complexes. To me this is evidence for the presence of VT as the QRS duration does not appear to be rate dependent as aberrency may be. I disagree that this could represent AIVR as, by definition the rate of AIVR is less than 100. A rate of over 100 of ventricular origin is, by defintion, VT. (1) Wellnes et. al. The Value of the Electrocardiogram in the Differential Diagnosis of a Tachycardia with a Widened QRS Complex. Am J Med 1978;64:27-33 (2) Akhtar et. al. Wide QRS Complex Tachycardia. Reapprisal of a Common Clincal Problem. Ann Int Med 1988;109:905-912 (3) Kindwall et. al. Electrocardiographic Criteria for Ventricular Tachycardia in Wide Complex Left Bundle Brabch Block Morphology Tachycardias. Am J Card 1988;61:1279-1283 (4) Brugada et. al. A New Approach to the Differential Diagnosis of a Regular Tachycardia With a Wide QRS Complex. Circulation 1991;83(5):1649-1659 (5) Baerman et. al. Differentiation of Ventricular Tachycardia From Supraventricular Tachycardia With Abberation: Value of the Clinical History. Ann Emer Med 1987;16:40-43 (6) Sager et. al. Wide Complex Tachycardias. Differential Diagnosis and Maangement. Card Clin 1991;9(4):595-618 (7) Levitt Supraventricular Tachycardia with Aberrant Conduction Versus Ventricular Tachycardia. Differentiation and Diagnosis. Am J Emer Med 1988;6(3):273-277 (8) Wrenn Management Strategies in Wide QRS Complex Tachycardia Am J Emerg Med 1991;9(6):592-597 This is an interesting question and I'll take another stab at it after having done a literature search. Although I have never seen this, I conceded that it was a possibility. Mikel suggested that the mechanism may be akin to the slowing that occurs in the AV node with high does of lidocaine but exerting it's effects, instead, upon the ventricular muscle. Not having carefully read his post I concluded that he was suggesting that lidocaine was slowing the ventricular rate in VT by it's effect on the AV node itself which was clearly not his intent. In fact, blocking of the sodium channel with lidocaine and increasing the VT cycle length before complete exit block and termination of the arrythymia occurs has been suggested as the mechanism of action (1). In human studies, procainamide and flecainide do prolong the cycle length of VT. Lidocaine although showing a trend in that direction as well does not do so in a statistically meaningful manner (2). On a chronic basis, group Ia drugs and amiodarone do result in a significant slowing of induced VT (3). Interestingly enough, VT with a longer cycle length appears to be easier to convert with overdrive pacing that that associated with faster rates (4). As an aside I noted an article on the use of transcutaneous overdrive pacing in the ED management of VT (5). H. Louzon MD (1) El-Sherif N, Scherlag BJ, Lazzara R, Hope RR Re-entrant ventricular arrhythmias in the late myocardial infarction period. 4. Mechanism of action of lidocaine. Circulation 1977 Sep;56(3):395-402 ABSTRACT: The effect of lidocaine on re-entrant ventricular arrhythmias (RVA) was studied in dogs 3-7 days following ligation of the anterior descending coronary artery; direct recordings were made of the re-entrant pathway (RP) from the epicardial surface of the infarction zone (IZ). Lidocaine in a therapeutic dose consistently prolonged refractoriness of potentially RP(s) in the IZ and produced a higher degree of conduction block at a constant heart rate. Conduction in the adjacent normal zone was not affected. The impairment of conduction induced by lidocaine in the RP was directly related to its ability to abolish re-entrant ventricular beats and tachycardia. Gradual slowing of conduction in the RP consistently developed before abolition: lengthening of coupling of extrasystolic beats in surface leads and gradual slowing of ventricular tachycardia rate occurred. The termination of re-entry was characteristically associated with complete block in the RP. A "selectivity hypothesis" for the antiarrhythmic action of lidocaine is proposed. (2) Kidwell GA, Greenspon AJ, Greenberg RM, Volosin KJ Use-dependent prolongation of ventricular tachycardia cycle length by type I antiarrhythmic drugs in humans. Circulation 1993 Jan;87(1):118-25 ABSTRACT: BACKGROUND. Type I antiarrhythmic drugs block the cardiac sodium channel in a use-dependent fashion. This use-dependent behavior causes increased drug binding and consequently increased sodium channel blockade at faster stimulation rates. Importantly, the kinetics of drug association and dissociation from the sodium channel differ for each type I antiarrhythmic drug. METHODS AND RESULTS. Thirty-five patients receiving type I antiarrhythmic drugs for the treatment of sustained monomorphic ventricular tachycardia (VT) were studied before and after drug therapy. A total of 41 drug studies were performed (lidocaine, n = 10; procainamide, n = 16; flecainide, n = 15). Sustained monomorphic VT of an identical electrocardiographic morphology was induced during the control and follow-up drug studies. During the control study, there was no significant change in the VT cycle length over time. Compared with control, significant prolongation of the onset VT cycle length was observed after treatment with procainamide and flecainide (increase of 52 +/- 24 and 80 +/- 49 msec, respectively) but not after treatment with lidocaine (increase of 8 +/- 37 msec). Additional drug-induced prolongation of the VT cycle length occurred during a 40-second observation period. This secondary "use-dependent" cycle length prolongation contributed significantly to the steady-state VT cycle length during treatment with flecainide (increase of 82 +/- 34 msec; p < 0.0001). Although a use-dependent increase in VT cycle length was observed with procainamide and lidocaine, the increase was not statistically significant (increase of 12 +/- 15 and 8 +/- 8 msec, respectively). The estimated time constants for the onset of use-dependent VT cycle length prolongation were distinctly different for the three drugs. Flecainide's prolongation of the VT cycle length occurred slowly, with an estimated time constant of 12.5 +/- 5.0 seconds. In contrast, the time course of VT cycle length prolongation was rapid during treatment with lidocaine and intermediate during treatment with procainamide (time constants of 0.52 +/- 0.51 and 4.0 +/- 1.3 seconds, respectively). CONCLUSIONS. Use-dependent prolongation of VT cycle length during treatment with type I antiarrhythmic drugs was observed in humans. This effect was clinically significant during treatment with flecainide (i.e., the use-dependent slowing of the heart rate improved the hemodynamic tolerance of the arrhythmia). Finally, the estimated time constants for the use-dependent prolongation of VT cycle length by the three test drugs are similar to their reported in vitro time constants for use-dependent sodium channel blockade. (3) Ferrick KJ, Singh S, Roth JA, Kim SG, Fisher JD Prediction of electrophysiologic study results in patients treated with amiodarone. Am Heart J 1995 Mar;129(3):496-501 ABSTRACT: To identify whether electrophysiologic study results during early-phase amiodarone therapy can be predicted by previous electrophysiologic study, we reviewed the electrophysiologic data of 50 patients with inducible sustained ventricular arrhythmias who underwent 4.3 +/- 1.3 drug trials before being given amiodarone. Study results during testing with agents of the modified Vaughan Williams Ia classification were compared with data obtained after 2 weeks of amiodarone therapy. Partial response by electrophysiologic study was defined as well-tolerated ventricular tachycardia < 150 beats/min associated with a blood pressure > or = 90 mm Hg. Significant slowing in the rate of induced ventricular tachycardia was seen during therapy with both Ia agents and amiodarone, although there was a trend toward greater slowing during amiodarone treatment (180 +/- 45 beats/min vs 164 +/- 65 beats/min; p = 0.09). Two of three patients with noninducible ventricular tachycardia during amiodarone showed profound ventricular tachycardia slowing during Ia therapy. Thirty-eight of 50 patients demonstrated concordance of electrophysiologic study results with regard to achieving partial response criteria. Twenty patients died during a mean follow-up period of 37 +/- 29 months; 7 of the 10 sudden deaths occurred in patients who did not meet partial response criteria. We conclude that patients with inducible sustained ventricular arrhythmias failing serial drug testing with Ia agents only rarely have their ventricular tachycardia suppressed during amiodarone therapy. Partial response criteria are often concordant between testing on agents of the Ia classification and amiodarone, and there was no significant difference in survival in patients based on their partial response status. (4) Keren G, Miura DS, Somberg JC Pacing termination of ventricular tachycardia: influence of antiarrhythmic-slowed ectopic rate. Am Heart J 1984 Apr;107(4):638-43 ABSTRACT: The success of pacing stimuli interruption of ventricular tachycardia (VT) was examined in 77 episodes of sustained VT induced in 31 patients undergoing programmed electrical stimulation studies. Once VT was induced, a trial to terminate the arrhythmia by means of the technique of entrainment was attempted. If this failed, rapid burst pacing faster than the VT was begun to try and terminate the tachycardia. In 30 patients off antiarrhythmic agents, entrainment was effective in terminating VT in 27%, while burst pacing was also effective in 27%. In 37% of patients, VT was accelerated or ventricular fibrillation was produced by pacing techniques, and these patients required defibrillation. Following antiarrhythmic therapy that failed to prevent VT induction but did result in slowing of VT rate, entrainment was only successful in 23% of trials, while burst pacing was successful in 34% of trials. The incidence of acceleration of VT on therapy was 32%. There was no appreciable difference in acceleration noted with or without antiarrhythmic therapy. Regardless of therapy, the slower the VT rate, the greater success of pacing termination of VT and the lower the incidence of VT acceleration. Antiarrhythmic agents that significantly slow the VT rate increase the success rate of pacing stimuli interruption of VT and decrease the incidence of VT acceleration and thus the need for defibrillation. The results suggest that antiarrhythmic agents that slow the VT rate may increase the effectiveness of antiarrhythmic pacemakers in terminating VT. (5) Grubb BP, Temesy-Armos P, Hahn H, Elliott L The use of external, noninvasive pacing for the termination of ventricular tachycardia in the emergency department setting. Department of Medicine, Medical College of Ohio, Toledo. Ann Emerg Med 1992 Feb;21(2):174-6 ABSTRACT: STUDY OBJECTIVE: To determine the potential usefulness of external cardiac pacing for the termination of sustained ventricular tachycardia in the emergency department setting. TYPE OF PARTICIPANTS: Five men and one woman (mean age, 57 years) who presented to the ED with a wide-complex, hemodynamically stable tachycardia that was later proven to be ventricular in origin. INTERVENTION: Each patient underwent external overdrive pacing using a modified external pacemaker at a pulse amplitude of 120 mA and a rate of 200 pulses per minute. RESULTS: In all six patients, external cardiac pacing was able to successfully terminate tachycardia without complication. CONCLUSION: We conclude that external noninvasive pacing may be an effective means of terminating ventricular tachycardia in the ED setting.