Grand Rounds Ventricular Tachycardia: Noninvasive Differentiation from Supraventricular Tachycardia
Henry J.L. Marriott, MD* Rogers Heart Foundation
The paramount importance of differentiating the wide-QRS tachycardias is stressed, and the alarming frequency of errors made by practicing physicians and cardiovascular nurses is documented. The most common causes of error are outlined, of which the most important is ignorance of diagnostically helpful QRS morphology in the electrocardiogram (EKG). The QRS contours and polarity that are useful in diagnosis are described in detail and illustrated. Finally, certain compromises in electrode placement that may be necessary in the operating room are suggested. Keywords: Tachycardia; myocardial infarction; electrocardiography; electrodes; atria1 fibrillation; arrhythmia; anesthesia; cardiology.
*Clinical Professor of Medicine (Cardiology), Emory University School of Medicine, Atlanta, GA; Clinical Professor of Pediatrics (Cardiology), University of Florida College of Medicine, Gainesville, FL; Director of Clinical Research and Education, Rogers Heart Foundation and St. Anthony’s Hospital Address reprint requests to Dr. Marriott at St. Anthony’s Hospital, P.O. Box 12588, St. Petersburg, FL 33733, USA. Received for publication July 19, 1989; cepted for publication August 7, 1989. 0 1990 Butterworth
Publishers
revised manuscript
ac-
and St. Anthony’s Hospital, St. Petersburg,
FL.
Introduction The most important electrocardiographic diagnosis that concerns all practitioners-cardiologists, internists, emergency room physicians, pediatricians, anesthesiologists, and surgeons-is determining the origin of the wide-QRS tachycardia. Does it originate in the ventricles, or does it arise above the ventricles and encounter delay in one of the bundle branches? The pendulum of misdiagnosis has swung interestingly over the past two decades. Formerly, the bizarre configuration of aberrantly conducted beats was mistaken for ventricular ectopy and treated with lidocaine. A patient would arrive in the emergency room with atria1 fibrillation and a rapid ventricular response punctuated by runs of bizarre beats that were mistaken for short bursts of ventricular tachycardia (VT). Lidocaine was administered, which favored A-V conduction. The ventricular rate therefore increased, the runs of supposed VT lengthened and invited more lidocaine, and a hazardous vicious circle was established. Although this scenario still undoubtedly happens, the current vogue is different and more serious. For some reason, there is a widespread inclination for practitioners confronted with VT to make a diagnosis of supraventricular tachycardia (SVT) with aberration.1-5 Verapamil is then administered, often with resulting hypotension and sometimes ventricular fibrillation.2-4 Regardless of which fashion is current, misdiJ. Clin. Anesth.,
vol.
2, Jan/Feb 1990
59
Grand Rounds agnosis endangers the patient, and it is clearly important to differentiate between VT and SVT with ventricular aberration. Misdiagnosis ranges from 39%3 to 96%,l and a recent survey of critical-care nurses uncovered a misdiagnosis rate of 78%.5
a
b
c
d
Common Sources of Error The first step toward accurate diagnosis is to avoid the five common sources of error (Table 1). In one study,’ the belief that VT could not be tolerated led to incorrect diagnosis in 96% of a subset of physicians. Although VT may be somewhat more likely to show slight irregularity, most cases of SVT (93%) and VT (79%) are regular. 6 Therefore, regularity is an unreliable index. Lead 2, which for decades has been widely favored as a monitoring lead, is one of the least discriminating. One reason is that the four common causes of a wide QRS (left and right bundle-branch block and left and right ventricular ectopy) can produce a similar (QS) pattern in lead 2 (Fipre 1). Clearly, a lead that can look the same in all four of the main causes of wide QRS is a poor selection for monitoring purposes. In the presence of a wide-QRS tachycardia, the detection of independent atria1 activity-either clinically or electrocardiographically-provides strong evidence in favor of VT, but it is often erroneously stressed as the linchpin of diagnosis. Unfortunately, most VTs do not show atria1 independence, for the following reasons: a small percentage of VTs are associated with atria1 fibrillation, and about 45% are blessed with retrograde conduction to the atria. Thus, A-V dissociation exists in perhaps 50% of all cases, but independent P waves are discernible in only about half of these (25% of the total). The atria1 independence may be clinically discernible-variation in intensity of the first heart sound and irregular cannon waves-in a few more. Independent atria1 activity is, therefore, useful as a clue in diagnosing about a third of all VTs at best. A greater source of error is neglect or ignorance of ectopic QRS morphology. Wellens et aZ.’demonstrated that 90% accuracy in diagnosis can be achieved
Table 1. Common Sources of Error 1. 2. 3. 4. 5.
60
Believing that VT cannot be hemodynamically tolerated Believing that VT is usually irregular Using lead 2 for diagnosis Depending on independent atria1 activity Ignorance of or disregard for morphologic clues
J. Clin. Anesth., vol. 2, Jan/Feb
1990
Figure 1. The four common causes of wide QRS: (a) right bundle-branch block; (b) left bundle-branch block; (c) right ventricular tachycardia; (d) left ventricular tachycardia. Note that all four conditions can sponsor a QS complex in lead 2.
from a study of QRS characteristics. No other method-except, of course, electrophysiologic studies-approaches this success rate. It is the duty of all physicians and all nurses who are called upon to make this differentiation to be familiar with all the available clues, but especially with those that require a knowledge of the differentiating QRS shapes. Despite this obligation, it is evident from several reports’-5 that the majority of physicians and critical-care nurses are ignorant of the nuances of QRS morphology. Before detailing the QRS clues available for making this important differential diagnosis, it is worth noting that a valuable pointer may be obtained from the patient’s history. Tchou et al.* suggested asking the following two questions: (1) Have you ever had a heart attack? and (2) Did your arrhythmia begin after the heart attack? If the answer to both of these questions is yes, a diagnosis of VT is almost certain.
The QRS Complex There is nothing new about the use of QRS shapes in differentiation. One would reasonably expect that there might be some subtle but recognizable differences between QRS complexes produced by activity originating in the ventricular myocardium and those produced by impulses arising above the ventricles and encountering a roadblock in their passage through the ventricles. The first intimation that this fact was true was in 1965 when attention was drawn to the fact that in lead V 1, most ectopic ventricular beats had a diphasic (qR) or monophasic (R) pattern, whereas right bundlebranch block (RBBB) beats tended to have a triphasic (rsR’ or rSR’) shape.g Since that time, observant clinicians,‘“-‘3 coronary-care nurses,14 and electrophysi-
Ventricular ectopy versus aberration: Marriott
ologists 6,7~15-21have amassed a formidable diagnostic clues with which all conscientious ticians should be familiar.
array of diagnos-
Obviously, the final court of appeal is the electrophysiologic laboratory, but this is an impractical, and often undesirable, resort in the majority of wide-QRS tachycardias encountered in daily practice. A noninvasive approach that affords 90% diagnostic accuracy is therefore worth adopting. There is no shortcut: The clues must be learned. Of the many available, those based on QRS morphology are paramount and are emphasized and illustrated here. One caveat: The QRS’s of Wolff-Parkinson-White conduction may be indistinguishable from ectopic ventricular QRS complexes. This fact is not surprising, since the accessory pathway delivers the atria1 impulse directly into ventricular myocardium, which is as though it originated in a ventricular focus situated at the distal end of the pathway. Fortunately, antidromic tachycardia--i.e., a circus-movement tachycardia whose circulating wavefront travels down an accessory pathway and up the A-V junction-is rare and seldom presents a diagnostic problem. However, many examples of atria1 fibrillation with accessory pathway conduction, despite the ventricular irregularity typical of atria1 fibrillation, have been mistaken for VT. For optimal diagnosis, a 12-lead tracing is obtained. Of the 12 leads, the most fruitful quartet consists of leads 1, aVF, Vl, and V6. Leads 1 and aVF indicate the frontal plane axis, and leads Vl and V6 provide requisite precordial information. Available clues are classifiable under the following headings: QRS morphology, QRS polarity, QRS duration, and A-V dissociation.
QRS Morphology Since there are two main mechanisms that produce a widened QRS (bundle-branch block, or BBB, and ectopy), if the widening is the result of BBB, the QRS pattern should be recognizably similar to one of the BBB patterns. At times in VT, the 12-lead QRS morphology resembles neither right nor left BBB (Figure 2), and in such cases, it is logical to conclude that the tachycardia is of ectopic ventricular origin.
Figure 2. A 124ead tracing of left ventricular tachycardia. Note the characteristic features: axis in right upper quadrant (“no-man’s-land”); monophasic R with early peak and slurring on downstroke in lead V 1; QS complex deeper than 15 mm in V6. Note also that the global pattern does not resemble either right or left bundle-branch block.
Figure 3. (a) In the middle of the strip, there is first a left and then a right ventricular extrasystole. The LV ectopic has a qR shape, with the left peak (“rabbit ear”) taller than the right. The RV ectopic has a slurred downstroke to a late nadir (>0.07 second). (b) The second beat is a left ventricular extrasystole with a single symmetrical peak. The flanking sinus beats are conducted with RBBB. (c) The right ventricular extrasystole has a fat (>0.03 second) r wave with a consequently delayed nadir (>0.07 second).
Global.
Single Lead. Lead VI
1. A diphasic (qR) or monophasic (R) complex favors left ventricular ectopy, especially if the left peak
(“rabbit ear”) is taller than the right (Figures 2 and 3a).
2. A single peak favors left ventricular
ectopy (Figure
3b).
3. A fat (>0.03 second) initial r (Figure 3~) or a slurring on the downstroke of the rS or QS (Figure 3a), in either case with the nadir reached late (BO.07 second), favors right ventricular ectopy. 4. A triphasic (rsR’ or rSR’) QRS favors RBBB aberration (Figure 4a). 5. An rS or QS with a slick downstroke and an earlier nadir (~0.07 second) favors LBBB aberration (Figure 4B).
J. Clin. Anesth.,
vol. 2, Jan/Feb
1990
61
Grand Rounds
Figure
4. (a) The
fifth beat signals the onset of a RBBB aberration complicating a supraventricular cardia. Note the rSR’ configuration. (b) With the beat, a run of LBBB aberration begins. Note the downstroke with slurring on the upstroke.
Figure 6. The diagnosis from MCL, is ambivalent, but the qRs configuration in MCL, establishes the diagnosis of incomplete RBBB aberration.
run of tachyfourth sheer
I
1
Figure
5. The first two beats are supraventricular with a typical (qRs) RBBB contour. The last four beats begin a run of left ventricular tachycardia. Note the absence of a Q wave, a small R wave, and a deep, wide S wave (>20 mm deep).
Lead V6 1. An t-S (Figure 5) or QS (Figure 2) favors ectopy, more
especially than
15 mm
2. A triphasic
if the negative deep
(qRs) pattern ration (Figures 5 and 6).
ventricular
(S or QS) wave is
(Figures 2 and 5).
favors an RBBB
aber-
Figure 7. (a) Left ventricular tachycardia manifesting positive concordance (upright QRS’s from Vl to V6). (b) Right ventricular tachycardia manifesting negative concordance (inverted QRS’s from Vl to V6).
ative concordance”; Figure 7b), ventricular ectopy is strongly favored. Caveat: Positive concordance is occasionally encountered in preexcitation with the uncommon antidromic tachycardia, and negative concordance is rarely seen in LBBB.
QRS Duration QRS Polarity The QRS axis most diagnostic of ventricular ectopy is in the right upper quadrant (“no-man’s_land”; Figure 1)-a predominantly negative deflection in leads 1 and aVF indicates an axis in this quadrant. In the presence of a positive QRS in V 1, marked axis deviation, either to the left or to the right, favors ventricular ectopy. Axis.
Wellens and coworker@J” found that the majority of VTs had QRS intervals in excess of 0.14 second, whereas most SVTs with aberrations had QRS intervals of 0.14 second or less. Caveat: This distinction can be invoked only if the patient is known not to have had preexisting BBB.
A-V Dissociation If all QRS’s are predominantly upright (“positive concordance”; Figure 7a) or inverted (“neg-
Concordance.
62
J. Clin. Anesth.,
vol. 2, Jan/Feb
1990
Three clues that should be considered together-because they are different expressions of the same phe-
Ventricular ectopy verse aberration: Marriott
nomenon (i.e., dissociated atria1 and ventricular activity)-are independent P waves, fusion beats, and early nonaberrant capture beats. All three are represented in Figure 8. Because A-V dissociation is likely to be present in only about half the patients with VT (in one series,lg it was present in only 27 of loo), it cannot be relied on for diagnosis. Moreover, it is readily detectable in only about half of those in whom it is present. Nevertheless, when present (Figure 8), independent atria1 activity affords extremely strong evidence in favor of VT because it is so rare to encounter a mimicking junctional tachycardia with not only BBB but also no retrograde conduction (and therefore an independent atria1 rhythm). Fusion beats (Figure 8) are informative when found. The argument goes like this: For fusion to occur within the ventricles, one impulse must have originated in the ventricles; therefore, fusion beats are diagnostic of ventricular ectopy. Unfortunately, as Kistinz2 demonstrated, it is possible for an atria1 impulse and an aberrantly conducted junctional impulse to fuse within the ventricles. A more important limitation of the fusion beat’s usefulness is the fact that fusion beats are seldom seen if the ventricular rate is much over 150/min, and most VTs have a rate in excess of 150/min. Nevertheless, when found, fusion beats are considered good evidence in favor of ventricular ectopy. The third clue, also dependent on A-V dissociation, is the early nonaberrant capture beat (Figure 8). If the capture beat interrupting the wide-QRS tachycardia (and ending a cycle shorter than that of the tachycardia) is normally narrow, it stands to reason that
Figure 8. Right ventricular tachycardia with three manifestations of A-V dissociation: independent P waves, several fusion beats (F), and early, nonaberrant capture beats (C). The first capture beat clearly contains an element of fusion and is therefore not a pure capture. Nevertheless, with its narrowed QRS, despite its prematurity, it serves the diagnostic purpose.
the wider (and longer) QRS ending cycles are unlikely to be aberrant and are therefore probably ectopic.
Surgical Constraints It is all very well to advocate the optimal leads for diagnosis, but how about the situation when the surgical field precludes ideal electrode placement? Whenever possible, the patient should be monitored with the positive electrode at the Vl positioni.e., close to the sternum in the fourth right interspace. If the negative electrode is placed at the left shoulder, the resulting lead (called MCLl and a popular lead for constant monitoring in intensive-care units) is the approximate equivalent of lead V 1. But in the presence of a median sternotomy, for example, this single best electrode site is out of bounds, and the practitioner must be resourceful and use the most fruitful deployment of electrodes available. In most surgical situations, it is possible to place an electrode in the left axilla, preferably in the midaxillary line at the level of the male nipple. This lead placement offers the advantages of VG-the rS or QS configurations of ectopy or the qRs of aberration. Another informative lead that can almost always be recorded is a standard lead 1, obtained by placing an electrode on both upper arms or on the two shoulders. Although this is not a good lead for recording P waves, in RBBB aberration it yields the telltale qRs shape. A deep, negative deflection indicates either marked right axis deviation or an axis in no-man’s_land, either of which is in favor of ventricular ectopy. With the positive electrode on the left leg (the left iliac crest is a satisfactory compromise), one can obtain an approximate lead 2 (if the negative electrode is at the right shoulder or upper arm) or lead 3 (if the negative electrode is at the left shoulder or upper arm) and so more firmly establish the frontal plane axis. If P waves are wanted, one of these “inferior” leads is most likely to proffer them. In an endeavor to obtain the desirable advantages of lead V 1, a distant approximation may be secured with the positive electrode in the right axilla, preferably in the mid-axillary line at the level of the male nipple. This lead, combined with that from the left axilla, indicates concordance when it is present. The width of the QRS may be measurable in any lead, and the clues related to A-V dissociation can be obtained from any lead that contains clearly defined P waves. Thus, even when ideal deployment is prohibited by the surgical procedure, an adequate harvest of diagnostic clues can usually be garnered by the resourceful monitor. J. Clin. Anesth., vol. 2, Jan/Feb
1990
63
Grand Rounds
Conclusion The wide-QRS tachycardias, though frequently misdiagnosed, are of great clinical importance and deserve detailed attention from every physician who may be called upon to handle urgent disturbances of cardiac rhythm. Accurate diagnosis cannot be achieved by guesswork, by intuition, or by the patient’s hemodynamic response to the tachycardia. With careful assessment of the clinical and electrocardiographic clues outlined above, there is no doubt that a correct diagnosis can be arrived at in the great majority of wide-QRS tachycardias, and the patient can thereby be protected from the dangers of inappropriate therapy.
References 1. Morady F, Baerman JM, DiCarlo LA, DeBuitleir M, Krol RB, Wahr DW: A prevalent misconception regarding wide-complex tachycardia. JAMA 1985; 254:2790-2. 2. Dancy M, Camm AJ, Ward D: Misdiagnosis of chronic Lancet 1985;2:320recurrent ventricular tachycardia. 3. 3. Stewart RB, Bardy GH, Greene HL: Wide complex tachycardia: misdiagnosis and outcome after emergent therapy. Ann Intern Med 1986; 104:766-7 1. RW, Olshansky B, Moreira D, 4. Switzer DF, Henthorn Waldo AL: Dire consequences of verapamil adminisCirculation 1986; tration for wide QRS tachycardias. 74(Suppl 2): 105. 5. Cooper J, Marriott HJL: Why are so many critical care nurses unable to recognize ventricular tachycardia in the 12-lead electrocardiogram? Heart Lung 1989; 18:2437. 6. Wellens HJJ, Bar FWHM, Lie KI: The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am J Med 1978;64:27-33. Wellens HJJ, Bar FW, Vanagt EJ, Brugada P, Farre J: The differentiation between ventricular tachycardia and supraventricular tachycardia with aberrant conduction: the value of the 12-lead electrocardiogram. In: Wellens HJJ, Kulbertus HE, eds. What’s New in Electrocardiography. Boston: Martinus Nijhoff, 198 1: 184-99. Tchou P, Young P, Mahmud R, Denker S, Jazayeri M, Akhtar M: Useful clinical criteria for the diagnosis of ventricular tachycardia. Am] Med 1988;84:53-56.
64
J. Clin. Anesth.,
vol. 2, Jan/Feb
1990
morphol9. Sandler IA, Marriott HJL: The differential ogy of anomalous ventricular complexes of RBBB-type in lead Vl: ventricular ectopy versus aberration. Circulation 1965;31:551-56. MB: Classification of ventricular extrasys10. Rosenbaum toles according to form. J Electrocardiol 1969;2:289-97. HJL: Differential diagnosis of supraventri11 Marriott cular and ventricular tachycardia. Geriatrics 1970;25:91101. with 12. Marriott HJL: Diagnosis of ventricular arrhythmias thoughts on therapy. Curr Ther Cardiovasc &ease 1984; 1:3-12. F, Marriott HJL: Morphologic 13. Swanick EJ, LaCamera features of right ventricular ectopic beats. Am.1 Cardiol 1972;30:888-91. D: Rabbit ears: an aid in distin14. Gozensky C, Thorne guishing ventricular ectopy from aberration. Heart Lung 1974;3:634-6. M, Wick15. Vera Z, Cheng TO, Ertem G, Shoaleh-var ramasekaran R, Wadhwa K: His bundle electrography for evaluation of criteria in differentiating ventricular ectopy from aberrance in atria1 fibrillation. Circulation 1972;45(Suppl 2):90. 16. Wellens HJJ, Bar FWHM, Vanagt EJDM, Brugada P: Medical treatment of ventricular tachycardia: considerations in the selection of patients for surgical treatment. Am J Cardiol 1982;49: 186-93. S, Yee R, Ko PT, Klein GJ: Electrocar17. Gulamhusein diographic criteria for differentiating aberrancy and ventricular extrasystole in chronic atria1 fibrillation: validation by intracardiac recordings. J Electrocardiol 1985;18:41-50. tach18. Wellens HJJ, Brugada P: Diagnosis of ventricular ycardia from the 12-lead electrocardiogram. Cardiol Clin 1987;5:51 l-25. 19. Niazi I, McKinney J, Caceres J, Jazayeri M, Tchou P, Akhtar M: Reevaluation of surface ECG criteria for the diagnosis of wide QRS tachycardia. Circulation 1987; 76(Suppl 4):412. KE, Brown J, Josephson M: Electrocardi20. Kindwall ographic criteria for ventricular tachycardia in wide complex left bundle branch morphology tachycardias. Am J Cardiol 1988;61:1279-83. 21 Akhtar M, Shenasa M, Jazayeri M, Caceres J, Tchou PJ: Wide QRS complex tachycardia: reappraisal of a common clinical problem. AnnIntern Med 1988; 109:90512. of ventric22. Kistin AD: Problems in the differentiation ular arrhythmia from supraventricular arrhythmia with abnormal QRS. Prog Cardiovasc Dis 1966;9: 1-12.
Henry J.L. Marriott, MD* Rogers Heart Foundation
The paramount importance of differentiating the wide-QRS tachycardias is stressed, and the alarming frequency of errors made by practicing physicians and cardiovascular nurses is documented. The most common causes of error are outlined, of which the most important is ignorance of diagnostically helpful QRS morphology in the electrocardiogram (EKG). The QRS contours and polarity that are useful in diagnosis are described in detail and illustrated. Finally, certain compromises in electrode placement that may be necessary in the operating room are suggested. Keywords: Tachycardia; myocardial infarction; electrocardiography; electrodes; atria1 fibrillation; arrhythmia; anesthesia; cardiology.
*Clinical Professor of Medicine (Cardiology), Emory University School of Medicine, Atlanta, GA; Clinical Professor of Pediatrics (Cardiology), University of Florida College of Medicine, Gainesville, FL; Director of Clinical Research and Education, Rogers Heart Foundation and St. Anthony’s Hospital Address reprint requests to Dr. Marriott at St. Anthony’s Hospital, P.O. Box 12588, St. Petersburg, FL 33733, USA. Received for publication July 19, 1989; cepted for publication August 7, 1989. 0 1990 Butterworth
Publishers
revised manuscript
ac-
and St. Anthony’s Hospital, St. Petersburg,
FL.
Introduction The most important electrocardiographic diagnosis that concerns all practitioners-cardiologists, internists, emergency room physicians, pediatricians, anesthesiologists, and surgeons-is determining the origin of the wide-QRS tachycardia. Does it originate in the ventricles, or does it arise above the ventricles and encounter delay in one of the bundle branches? The pendulum of misdiagnosis has swung interestingly over the past two decades. Formerly, the bizarre configuration of aberrantly conducted beats was mistaken for ventricular ectopy and treated with lidocaine. A patient would arrive in the emergency room with atria1 fibrillation and a rapid ventricular response punctuated by runs of bizarre beats that were mistaken for short bursts of ventricular tachycardia (VT). Lidocaine was administered, which favored A-V conduction. The ventricular rate therefore increased, the runs of supposed VT lengthened and invited more lidocaine, and a hazardous vicious circle was established. Although this scenario still undoubtedly happens, the current vogue is different and more serious. For some reason, there is a widespread inclination for practitioners confronted with VT to make a diagnosis of supraventricular tachycardia (SVT) with aberration.1-5 Verapamil is then administered, often with resulting hypotension and sometimes ventricular fibrillation.2-4 Regardless of which fashion is current, misdiJ. Clin. Anesth.,
vol.
2, Jan/Feb 1990
59
Grand Rounds agnosis endangers the patient, and it is clearly important to differentiate between VT and SVT with ventricular aberration. Misdiagnosis ranges from 39%3 to 96%,l and a recent survey of critical-care nurses uncovered a misdiagnosis rate of 78%.5
a
b
c
d
Common Sources of Error The first step toward accurate diagnosis is to avoid the five common sources of error (Table 1). In one study,’ the belief that VT could not be tolerated led to incorrect diagnosis in 96% of a subset of physicians. Although VT may be somewhat more likely to show slight irregularity, most cases of SVT (93%) and VT (79%) are regular. 6 Therefore, regularity is an unreliable index. Lead 2, which for decades has been widely favored as a monitoring lead, is one of the least discriminating. One reason is that the four common causes of a wide QRS (left and right bundle-branch block and left and right ventricular ectopy) can produce a similar (QS) pattern in lead 2 (Fipre 1). Clearly, a lead that can look the same in all four of the main causes of wide QRS is a poor selection for monitoring purposes. In the presence of a wide-QRS tachycardia, the detection of independent atria1 activity-either clinically or electrocardiographically-provides strong evidence in favor of VT, but it is often erroneously stressed as the linchpin of diagnosis. Unfortunately, most VTs do not show atria1 independence, for the following reasons: a small percentage of VTs are associated with atria1 fibrillation, and about 45% are blessed with retrograde conduction to the atria. Thus, A-V dissociation exists in perhaps 50% of all cases, but independent P waves are discernible in only about half of these (25% of the total). The atria1 independence may be clinically discernible-variation in intensity of the first heart sound and irregular cannon waves-in a few more. Independent atria1 activity is, therefore, useful as a clue in diagnosing about a third of all VTs at best. A greater source of error is neglect or ignorance of ectopic QRS morphology. Wellens et aZ.’demonstrated that 90% accuracy in diagnosis can be achieved
Table 1. Common Sources of Error 1. 2. 3. 4. 5.
60
Believing that VT cannot be hemodynamically tolerated Believing that VT is usually irregular Using lead 2 for diagnosis Depending on independent atria1 activity Ignorance of or disregard for morphologic clues
J. Clin. Anesth., vol. 2, Jan/Feb
1990
Figure 1. The four common causes of wide QRS: (a) right bundle-branch block; (b) left bundle-branch block; (c) right ventricular tachycardia; (d) left ventricular tachycardia. Note that all four conditions can sponsor a QS complex in lead 2.
from a study of QRS characteristics. No other method-except, of course, electrophysiologic studies-approaches this success rate. It is the duty of all physicians and all nurses who are called upon to make this differentiation to be familiar with all the available clues, but especially with those that require a knowledge of the differentiating QRS shapes. Despite this obligation, it is evident from several reports’-5 that the majority of physicians and critical-care nurses are ignorant of the nuances of QRS morphology. Before detailing the QRS clues available for making this important differential diagnosis, it is worth noting that a valuable pointer may be obtained from the patient’s history. Tchou et al.* suggested asking the following two questions: (1) Have you ever had a heart attack? and (2) Did your arrhythmia begin after the heart attack? If the answer to both of these questions is yes, a diagnosis of VT is almost certain.
The QRS Complex There is nothing new about the use of QRS shapes in differentiation. One would reasonably expect that there might be some subtle but recognizable differences between QRS complexes produced by activity originating in the ventricular myocardium and those produced by impulses arising above the ventricles and encountering a roadblock in their passage through the ventricles. The first intimation that this fact was true was in 1965 when attention was drawn to the fact that in lead V 1, most ectopic ventricular beats had a diphasic (qR) or monophasic (R) pattern, whereas right bundlebranch block (RBBB) beats tended to have a triphasic (rsR’ or rSR’) shape.g Since that time, observant clinicians,‘“-‘3 coronary-care nurses,14 and electrophysi-
Ventricular ectopy versus aberration: Marriott
ologists 6,7~15-21have amassed a formidable diagnostic clues with which all conscientious ticians should be familiar.
array of diagnos-
Obviously, the final court of appeal is the electrophysiologic laboratory, but this is an impractical, and often undesirable, resort in the majority of wide-QRS tachycardias encountered in daily practice. A noninvasive approach that affords 90% diagnostic accuracy is therefore worth adopting. There is no shortcut: The clues must be learned. Of the many available, those based on QRS morphology are paramount and are emphasized and illustrated here. One caveat: The QRS’s of Wolff-Parkinson-White conduction may be indistinguishable from ectopic ventricular QRS complexes. This fact is not surprising, since the accessory pathway delivers the atria1 impulse directly into ventricular myocardium, which is as though it originated in a ventricular focus situated at the distal end of the pathway. Fortunately, antidromic tachycardia--i.e., a circus-movement tachycardia whose circulating wavefront travels down an accessory pathway and up the A-V junction-is rare and seldom presents a diagnostic problem. However, many examples of atria1 fibrillation with accessory pathway conduction, despite the ventricular irregularity typical of atria1 fibrillation, have been mistaken for VT. For optimal diagnosis, a 12-lead tracing is obtained. Of the 12 leads, the most fruitful quartet consists of leads 1, aVF, Vl, and V6. Leads 1 and aVF indicate the frontal plane axis, and leads Vl and V6 provide requisite precordial information. Available clues are classifiable under the following headings: QRS morphology, QRS polarity, QRS duration, and A-V dissociation.
QRS Morphology Since there are two main mechanisms that produce a widened QRS (bundle-branch block, or BBB, and ectopy), if the widening is the result of BBB, the QRS pattern should be recognizably similar to one of the BBB patterns. At times in VT, the 12-lead QRS morphology resembles neither right nor left BBB (Figure 2), and in such cases, it is logical to conclude that the tachycardia is of ectopic ventricular origin.
Figure 2. A 124ead tracing of left ventricular tachycardia. Note the characteristic features: axis in right upper quadrant (“no-man’s-land”); monophasic R with early peak and slurring on downstroke in lead V 1; QS complex deeper than 15 mm in V6. Note also that the global pattern does not resemble either right or left bundle-branch block.
Figure 3. (a) In the middle of the strip, there is first a left and then a right ventricular extrasystole. The LV ectopic has a qR shape, with the left peak (“rabbit ear”) taller than the right. The RV ectopic has a slurred downstroke to a late nadir (>0.07 second). (b) The second beat is a left ventricular extrasystole with a single symmetrical peak. The flanking sinus beats are conducted with RBBB. (c) The right ventricular extrasystole has a fat (>0.03 second) r wave with a consequently delayed nadir (>0.07 second).
Global.
Single Lead. Lead VI
1. A diphasic (qR) or monophasic (R) complex favors left ventricular ectopy, especially if the left peak
(“rabbit ear”) is taller than the right (Figures 2 and 3a).
2. A single peak favors left ventricular
ectopy (Figure
3b).
3. A fat (>0.03 second) initial r (Figure 3~) or a slurring on the downstroke of the rS or QS (Figure 3a), in either case with the nadir reached late (BO.07 second), favors right ventricular ectopy. 4. A triphasic (rsR’ or rSR’) QRS favors RBBB aberration (Figure 4a). 5. An rS or QS with a slick downstroke and an earlier nadir (~0.07 second) favors LBBB aberration (Figure 4B).
J. Clin. Anesth.,
vol. 2, Jan/Feb
1990
61
Grand Rounds
Figure
4. (a) The
fifth beat signals the onset of a RBBB aberration complicating a supraventricular cardia. Note the rSR’ configuration. (b) With the beat, a run of LBBB aberration begins. Note the downstroke with slurring on the upstroke.
Figure 6. The diagnosis from MCL, is ambivalent, but the qRs configuration in MCL, establishes the diagnosis of incomplete RBBB aberration.
run of tachyfourth sheer
I
1
Figure
5. The first two beats are supraventricular with a typical (qRs) RBBB contour. The last four beats begin a run of left ventricular tachycardia. Note the absence of a Q wave, a small R wave, and a deep, wide S wave (>20 mm deep).
Lead V6 1. An t-S (Figure 5) or QS (Figure 2) favors ectopy, more
especially than
15 mm
2. A triphasic
if the negative deep
(qRs) pattern ration (Figures 5 and 6).
ventricular
(S or QS) wave is
(Figures 2 and 5).
favors an RBBB
aber-
Figure 7. (a) Left ventricular tachycardia manifesting positive concordance (upright QRS’s from Vl to V6). (b) Right ventricular tachycardia manifesting negative concordance (inverted QRS’s from Vl to V6).
ative concordance”; Figure 7b), ventricular ectopy is strongly favored. Caveat: Positive concordance is occasionally encountered in preexcitation with the uncommon antidromic tachycardia, and negative concordance is rarely seen in LBBB.
QRS Duration QRS Polarity The QRS axis most diagnostic of ventricular ectopy is in the right upper quadrant (“no-man’s_land”; Figure 1)-a predominantly negative deflection in leads 1 and aVF indicates an axis in this quadrant. In the presence of a positive QRS in V 1, marked axis deviation, either to the left or to the right, favors ventricular ectopy. Axis.
Wellens and coworker@J” found that the majority of VTs had QRS intervals in excess of 0.14 second, whereas most SVTs with aberrations had QRS intervals of 0.14 second or less. Caveat: This distinction can be invoked only if the patient is known not to have had preexisting BBB.
A-V Dissociation If all QRS’s are predominantly upright (“positive concordance”; Figure 7a) or inverted (“neg-
Concordance.
62
J. Clin. Anesth.,
vol. 2, Jan/Feb
1990
Three clues that should be considered together-because they are different expressions of the same phe-
Ventricular ectopy verse aberration: Marriott
nomenon (i.e., dissociated atria1 and ventricular activity)-are independent P waves, fusion beats, and early nonaberrant capture beats. All three are represented in Figure 8. Because A-V dissociation is likely to be present in only about half the patients with VT (in one series,lg it was present in only 27 of loo), it cannot be relied on for diagnosis. Moreover, it is readily detectable in only about half of those in whom it is present. Nevertheless, when present (Figure 8), independent atria1 activity affords extremely strong evidence in favor of VT because it is so rare to encounter a mimicking junctional tachycardia with not only BBB but also no retrograde conduction (and therefore an independent atria1 rhythm). Fusion beats (Figure 8) are informative when found. The argument goes like this: For fusion to occur within the ventricles, one impulse must have originated in the ventricles; therefore, fusion beats are diagnostic of ventricular ectopy. Unfortunately, as Kistinz2 demonstrated, it is possible for an atria1 impulse and an aberrantly conducted junctional impulse to fuse within the ventricles. A more important limitation of the fusion beat’s usefulness is the fact that fusion beats are seldom seen if the ventricular rate is much over 150/min, and most VTs have a rate in excess of 150/min. Nevertheless, when found, fusion beats are considered good evidence in favor of ventricular ectopy. The third clue, also dependent on A-V dissociation, is the early nonaberrant capture beat (Figure 8). If the capture beat interrupting the wide-QRS tachycardia (and ending a cycle shorter than that of the tachycardia) is normally narrow, it stands to reason that
Figure 8. Right ventricular tachycardia with three manifestations of A-V dissociation: independent P waves, several fusion beats (F), and early, nonaberrant capture beats (C). The first capture beat clearly contains an element of fusion and is therefore not a pure capture. Nevertheless, with its narrowed QRS, despite its prematurity, it serves the diagnostic purpose.
the wider (and longer) QRS ending cycles are unlikely to be aberrant and are therefore probably ectopic.
Surgical Constraints It is all very well to advocate the optimal leads for diagnosis, but how about the situation when the surgical field precludes ideal electrode placement? Whenever possible, the patient should be monitored with the positive electrode at the Vl positioni.e., close to the sternum in the fourth right interspace. If the negative electrode is placed at the left shoulder, the resulting lead (called MCLl and a popular lead for constant monitoring in intensive-care units) is the approximate equivalent of lead V 1. But in the presence of a median sternotomy, for example, this single best electrode site is out of bounds, and the practitioner must be resourceful and use the most fruitful deployment of electrodes available. In most surgical situations, it is possible to place an electrode in the left axilla, preferably in the midaxillary line at the level of the male nipple. This lead placement offers the advantages of VG-the rS or QS configurations of ectopy or the qRs of aberration. Another informative lead that can almost always be recorded is a standard lead 1, obtained by placing an electrode on both upper arms or on the two shoulders. Although this is not a good lead for recording P waves, in RBBB aberration it yields the telltale qRs shape. A deep, negative deflection indicates either marked right axis deviation or an axis in no-man’s_land, either of which is in favor of ventricular ectopy. With the positive electrode on the left leg (the left iliac crest is a satisfactory compromise), one can obtain an approximate lead 2 (if the negative electrode is at the right shoulder or upper arm) or lead 3 (if the negative electrode is at the left shoulder or upper arm) and so more firmly establish the frontal plane axis. If P waves are wanted, one of these “inferior” leads is most likely to proffer them. In an endeavor to obtain the desirable advantages of lead V 1, a distant approximation may be secured with the positive electrode in the right axilla, preferably in the mid-axillary line at the level of the male nipple. This lead, combined with that from the left axilla, indicates concordance when it is present. The width of the QRS may be measurable in any lead, and the clues related to A-V dissociation can be obtained from any lead that contains clearly defined P waves. Thus, even when ideal deployment is prohibited by the surgical procedure, an adequate harvest of diagnostic clues can usually be garnered by the resourceful monitor. J. Clin. Anesth., vol. 2, Jan/Feb
1990
63
Grand Rounds
Conclusion The wide-QRS tachycardias, though frequently misdiagnosed, are of great clinical importance and deserve detailed attention from every physician who may be called upon to handle urgent disturbances of cardiac rhythm. Accurate diagnosis cannot be achieved by guesswork, by intuition, or by the patient’s hemodynamic response to the tachycardia. With careful assessment of the clinical and electrocardiographic clues outlined above, there is no doubt that a correct diagnosis can be arrived at in the great majority of wide-QRS tachycardias, and the patient can thereby be protected from the dangers of inappropriate therapy.
References 1. Morady F, Baerman JM, DiCarlo LA, DeBuitleir M, Krol RB, Wahr DW: A prevalent misconception regarding wide-complex tachycardia. JAMA 1985; 254:2790-2. 2. Dancy M, Camm AJ, Ward D: Misdiagnosis of chronic Lancet 1985;2:320recurrent ventricular tachycardia. 3. 3. Stewart RB, Bardy GH, Greene HL: Wide complex tachycardia: misdiagnosis and outcome after emergent therapy. Ann Intern Med 1986; 104:766-7 1. RW, Olshansky B, Moreira D, 4. Switzer DF, Henthorn Waldo AL: Dire consequences of verapamil adminisCirculation 1986; tration for wide QRS tachycardias. 74(Suppl 2): 105. 5. Cooper J, Marriott HJL: Why are so many critical care nurses unable to recognize ventricular tachycardia in the 12-lead electrocardiogram? Heart Lung 1989; 18:2437. 6. Wellens HJJ, Bar FWHM, Lie KI: The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am J Med 1978;64:27-33. Wellens HJJ, Bar FW, Vanagt EJ, Brugada P, Farre J: The differentiation between ventricular tachycardia and supraventricular tachycardia with aberrant conduction: the value of the 12-lead electrocardiogram. In: Wellens HJJ, Kulbertus HE, eds. What’s New in Electrocardiography. Boston: Martinus Nijhoff, 198 1: 184-99. Tchou P, Young P, Mahmud R, Denker S, Jazayeri M, Akhtar M: Useful clinical criteria for the diagnosis of ventricular tachycardia. Am] Med 1988;84:53-56.
64
J. Clin. Anesth.,
vol. 2, Jan/Feb
1990
morphol9. Sandler IA, Marriott HJL: The differential ogy of anomalous ventricular complexes of RBBB-type in lead Vl: ventricular ectopy versus aberration. Circulation 1965;31:551-56. MB: Classification of ventricular extrasys10. Rosenbaum toles according to form. J Electrocardiol 1969;2:289-97. HJL: Differential diagnosis of supraventri11 Marriott cular and ventricular tachycardia. Geriatrics 1970;25:91101. with 12. Marriott HJL: Diagnosis of ventricular arrhythmias thoughts on therapy. Curr Ther Cardiovasc &ease 1984; 1:3-12. F, Marriott HJL: Morphologic 13. Swanick EJ, LaCamera features of right ventricular ectopic beats. Am.1 Cardiol 1972;30:888-91. D: Rabbit ears: an aid in distin14. Gozensky C, Thorne guishing ventricular ectopy from aberration. Heart Lung 1974;3:634-6. M, Wick15. Vera Z, Cheng TO, Ertem G, Shoaleh-var ramasekaran R, Wadhwa K: His bundle electrography for evaluation of criteria in differentiating ventricular ectopy from aberrance in atria1 fibrillation. Circulation 1972;45(Suppl 2):90. 16. Wellens HJJ, Bar FWHM, Vanagt EJDM, Brugada P: Medical treatment of ventricular tachycardia: considerations in the selection of patients for surgical treatment. Am J Cardiol 1982;49: 186-93. S, Yee R, Ko PT, Klein GJ: Electrocar17. Gulamhusein diographic criteria for differentiating aberrancy and ventricular extrasystole in chronic atria1 fibrillation: validation by intracardiac recordings. J Electrocardiol 1985;18:41-50. tach18. Wellens HJJ, Brugada P: Diagnosis of ventricular ycardia from the 12-lead electrocardiogram. Cardiol Clin 1987;5:51 l-25. 19. Niazi I, McKinney J, Caceres J, Jazayeri M, Tchou P, Akhtar M: Reevaluation of surface ECG criteria for the diagnosis of wide QRS tachycardia. Circulation 1987; 76(Suppl 4):412. KE, Brown J, Josephson M: Electrocardi20. Kindwall ographic criteria for ventricular tachycardia in wide complex left bundle branch morphology tachycardias. Am J Cardiol 1988;61:1279-83. 21 Akhtar M, Shenasa M, Jazayeri M, Caceres J, Tchou PJ: Wide QRS complex tachycardia: reappraisal of a common clinical problem. AnnIntern Med 1988; 109:90512. of ventric22. Kistin AD: Problems in the differentiation ular arrhythmia from supraventricular arrhythmia with abnormal QRS. Prog Cardiovasc Dis 1966;9: 1-12.
