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Transcript
9 6 Broad QRS Tachycardias Hein J.J. Wellens Recognition of Atrioventricular Dissociation. . . . . . . . Mechanisms of Widened QRS During Supraventricular Tachycardia . . . . . . . . . . . . . . . . . . Electrocardiographic Diagnosis of Wide QRS Tachycardia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Configurational Characteristics of the QRS Complex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2007 2008 2009 Localizing the Site of Origin of Ventricular Tachycardia . . . . . . . . . . . . . . . . . . . . . . Etiology of Ventricular Tachycardia. . . . . . . . . . . . . . . . Value of the ECG During Sinus Rhythm . . . . . . . . . . . The Practical Approach . . . . . . . . . . . . . . . . . . . . . . . . . . Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2012 2014 2016 2017 2017 2011 Key Points • Ninety percent of broad QRS tachycardia patients presenting to the emergency room are ventricular tachycardias (VTs). • Atrioventricular dissociation in VT is characterized by irregular cannon A waves in the jugular venous pulse, varying intensity of the first heart sound, beat-to-beat changes in the systolic blood pressure. • Independent beating of atria and ventricles during VT can result in “capture” or “fusion beats.” • Ninety percent of cases of VT have a QRS duration of more than 0.14 second and virtually all supraventricular tachycardias (SVTs) with aberrant conduction have a QRS duration of <0.14 second. • Most VTs have a prior myocardial infarction as their etiology. • Idiopathic VTs may have their origin in the RV or LV. • When a wide QRS tachycardia is not tolerated hemodynamically, emergent cardioversion should be performed. Because a drug given for the treatment of supraventricular tachycardia (SVT) may be deleterious to a patient with a ventricular tachycardia (VT),1,2 the differential diagnosis in broad QRS tachycardia is critical. Although 90% of broad QRS tachycardias presenting in the emergency room are VT, errors are often made because physicians wrongly consider VT unlikely if the patient is hemodynamically stable,3 and they are frequently unaware that certain findings on physical examination and on the electrocardiogram (ECG) may quickly and accurately lead to the correct diagnosis. The possible causes of a broad (wide) QRS tachycardia are as follows (corresponding to A to F in Fig. 96.1): 1. Supraventricular tachycardia with preexisting or functional bundle branch block (BBB). This includes sinus tachy- cardia, atrial tachycardia, atrial flutter, atrial fibrillation, and atrioventricular (AV) nodal reentrant tachycardia. 2. Orthodromic circus movement tachycardia using the AV node in the anterograde direction and an accessory pathway in the retrograde direction with preexisting or functional BBB. 3. Supraventricular tachycardia with conduction over an accessory AV pathway. 4. Antidromic circus movement tachycardia using an accessory pathway in the anterograde direction and the AV node or another accessory pathway in the retrograde direction. 5. Atrioventricular reentrant tachycardia using a nodoventricular fiber in the anterograde direction and the bundle of His or another accessory pathway in the retrograde direction. 6. Ventricular tachycardia. Recognition of Atrioventricular Dissociation In addition to careful evaluation of the ECG, examination of the patient should include a search for physical signs of AV dissociation. Atrioventricular dissociation is present in approximately 50% of all VTs. The other 50% show some form of retrograde conduction to the atria.4 Therefore, the finding of AV dissociation is an important diagnostic clue. The physical signs of AV dissociation are as follows5: 1. Irregular cannon A waves in the jugular pulse 2. Varying intensity of the first heart sound 3. Beat-to-beat changes in systolic blood pressure Any one of these three clues indicates AV dissociation. However, in the absence of such clues, VT cannot be ruled out; there remains the possibility of coexistent atrial 20 07 CAR096.indd 2007 11/24/2006 1:33:16 PM 2008 chapter 96 Mechanisms of Widened QRS During Supraventricular Tachycardia As shown in Figure 96.1, BBB may be one of the causes of a wide QRS tachycardia. This block may be preexistent (also present during sinus rhythm) or functional. Functional BBB during SVT may occur because of phase 3 block or retrograde invasion into the bundle branch. Phase 3 Block FIGURE 96.1. Possible causes of wide QRS tachycardia. See text for explanation. fibrillation or ventriculoatrial conduction, in which case none of the signs of AV dissociation would be present. In theory, it is also possible for an AV junctional tachycardia with retrograde block to have AV dissociation; however, in view of the rarity of such a rhythm, AV dissociation remains a valuable diagnostic clue for VT. The Jugular Pulse In VT with independent beating of atria and ventricles, the atria occasionally beat against closed AV valves, resulting in retrograde blood flow into the jugular vein, producing the so-called cannon A wave. Inspection of the jugular vein reveals the characteristic occasional expansive pulsation. Phase 3 (tachycardia-dependent) aberration usually occurs in the right bundle branch because that bundle commonly has the longest refractory period.6 Left bundle branch block (LBBB) aberration accounts for approximately one third of cases of aberrant ventricular conduction. It may occur in normal fiber if the impulse is premature enough to reach the cell when the membrane has not fully repolarized. This form of aberration is commonly observed at the beginning of paroxysmal SVT (Fig. 96.2). Phase 3 aberration is promoted by a long-short cycle sequence because the refractory period of the bundle branch of the beat following the long cycle is prolonged. Concealed Retrograde Conduction Although the mechanism of QRS widening at the onset of SVT commonly is phase 3 aberration, the sustaining mechanism is often concealed retrograde conduction up one of the bundle branches.6,7 Figure 96.3 is a schematic representation of how, during sinus rhythm, LBBB aberration is initiated by the premature atrial beat that also initiates SVT. This phase 3 block of the left bundle is followed by conduction over the right bundle and retrograde invasion into the left bundle branch. This makes the left bundle branch refractory when the next supraventricular impulse passes through the AV node. The impulse is conducted down the right bundle branch and then in a retrograde direction again up the left bundle branch. This mechanism is responsible for continua- Varying Intensity of the First Heart Sound The first heart sound marks the onset of ventricular systole and is caused by the closing of the mitral and tricuspid valves. During AV dissociation, there is a beat-to-beat change in the loudness of the first heart sound, owing to the varying position of the AV valves at the time of ventricular contraction. Therefore, the first heart sound varies in intensity during VT and in complete heart block, as well as during AV Wenckebach and atrial fibrillation. 82337 II III V1 Changes in Systolic Blood Pressure During AV dissociation, ventricular filling from the atria varies, depending on the time interval between atrial and ventricular contraction. These differences in ventricular filling lead to a beat-to-beat change in systolic stroke volume into the aorta, which in turn causes beat-to-beat changes in systolic blood pressure. This sign of AV dissociation can easily be detected at the bedside by use of the blood pressure recorder. Thus, a typical fi nding in VT with AV dissociation is that the rhythm is regular, whereas the systolic blood pressure differs from beat to beat. CAR096.indd 2008 V4 V6 400 ms FIGURE 96.2. Phase 3 aberration. In a patient with supraventricular tachycardia (SVT) and 2 : 1 atrioventricular (AV) conduction (left), there is a sudden change in 1 : 1 AV conduction. This sudden increase in ventricular rate is accompanied by widening of the fi rst three QRS complexes (left bundle branch block, LBBB). Note that the third QRS shows less widening than the first and second QRS complexes. This sequence is typical of phase 3 aberration. 11/24/2006 1:33:16 PM broa d qr s tach yc a r di a s 2009 Retrograde concealed conduction into one of the bundle branches is a common mechanism of perpetuation of aberration during SVT.6 His RBB Electrocardiographic Diagnosis of Wide QRS Tachycardia LBB A A 12-lead ECG is required for the correct diagnosis of wide QRS tachycardia on the basis of morphology. The physician should examine the ECG systematically, looking for the presence of AV dissociation and analyzing QRS characteristics, such as width, axis, and configuration. Atrioventricular Dissociation B FIGURE 96.3. (A,B) Schematic representation of initiation of left bundle branch (LBB) block aberration and perpetuation of aberration by concealed retrograde invasion into the left bundle branch. These critical time relations are interrupted by a ventricular premature beat resulting in normalization of the QRS complex during the SVT. tion of LBBB during SVT. Retrograde invasion into the left bundle branch continues until it is disrupted by a ventricular premature beat. Figure 96.4 gives a clinical example of the latter mechanism during SVT with right bundle branch block. A B Traditionally (and correctly), dissociation between atrial and ventricular activity during tachycardia has been considered a hallmark of VT. As pointed out previously, however,4 some form of ventriculoatrial conduction is frequently present during VT. Identification of atrial activity during VT can be difficult or impossible on the 12-lead ECG. Recognition of the P wave in a wide QRS tachycardia is important, however, because of the diagnostic value of AV dissociation. Independent beating of atria and ventricles during a VT can result in “capture” or “fusion” complexes (Fig. 96.5). This occurs when the ventricular rate during VT is such that an appropriately timed atrial impulse is able to traverse the AV node to depolarize the ventricles completely (capture) or partially (fusion). In the latter situation, fusion occurs because of concomitant ventricular activation from the VT focus (Fig. 96.5). 85499 99571 I I II II III aVR III aVR aVL aVL aVF V1 V2 V3 V4 aVF V1 V2 V3 V4 V5 V5 V6 400 ms 85473 FIGURE 96.4. (A) Example of widening of the QRS complex during tachycardia by retrograde invasion into the right bundle branch. The critical time relations required for perpetuation of retrograde invasion into the right bundle branch are disrupted by a right-sided ventricular premature beat. (B) Same patient during sinus rhythm. CAR096.indd 2009 V6 991203 400 ms FIGURE 96.5. An example of a ventricular tachycardia with ventricular fusion and capture beats. The narrow QRS complex of beat 5, is a fusion complex. The last narrow QRS complex during the tachycardia terminates VT because of invasion into the reentry circuit of the VT. Note that the patient has extensive scarring of the anterior wall from a previous myocardial infarction. 11/24/2006 1:33:17 PM 2 010 chapter I aVR V1 V4 II aVL V2 V5 III aVF V3 V6 96 V1 II FIGURE 96.6. Marked widening of the QRS in a patient with an atrial tachycardia who is on flecainide medication. V5 The occurrence of a narrower QRS during VT is not always the result of a conducted supraventricular beat; it may also result from fusion with a ventricular depolarization arising in the ventricle contralateral to the ventricle in which the tachycardia originates, or when fusion occurs with a ventricular echo beat when a retrogradely conducted impulse during VT travels to the AV node and reenters the ventricle.8 a right axis deviation is very likely to be VT. In discussing the importance of the axis in the frontal plane in the differential diagnosis of wide QRS tachycardia, it is important to realize that a markedly abnormal axis can occur in A B I I II II 05019 Width of the QRS Complex When we compared the width of the QRS complex in 100 cases of VT and 100 cases of SVT with aberrant conduction, we found that all cases of SVT with aberrant conduction had a QRS width of less than or equal to 0.14 second, whereas 95% of cases of VT had a QRS width of more than 0.14 second.4 These findings indicate that a QRS width of more than 0.14 second is highly suggestive of a ventricular origin of the tachycardia. The cause of a VT also plays a role in the width of the QRS complex. As reported by Coumel and associates9 in coronary artery disease, the average QRS complex is wider during VT than the QRS complex of the patient with idiopathic VT (171 vs. 135 ms). There are three situations in which an SVT can have a QRS width of more than 0.14 second. The first occurs when the patient has an SVT in the presence of preexistent bundle branch block. The second involves an SVT with AV conduction over an accessory pathway. The third is marked QRS widening during SVT because of the use of antiarrhythmic drugs that prolong intraventricular conduction, most commonly flecainide. A typical example of the latter is given in Figure 96.6. III III aVR aVR aVL aVL aVF V1 V1 V2 V2 V3 Most patients with VT secondary to a previous myocardial infarction have a markedly abnormal QRS axis in the frontal plane. Especially in right bundle branch block (RBBB)-like VT, the axis usually points superiorly, in contrast to SVT with RBBB, in which the axis is to the right. Patients with idiopathic VT can have a normal QRS axis in the frontal plane, but the two most common types of idiopathic VT may have marked left-axis or right-axis deviation (Fig. 96.7). In fact, an LBBB-shaped tachycardia with a vertical axis or CAR096.indd 2010 V3 V4 V4 The QRS Axis aVF V5 V5 V6 V6 400 ms FIGURE 96.7. The two most common forms of idiopathic ventricular tachycardia. (A) The origin is in the outflow tract of the right ventricle. The QRS shows an LBBB-shaped QRS and a vertical axis. (B) The origin is in the inferoseptal portion of the left ventricle. The QRS shows a right bundle branch block (RBBB) shape and left axis deviation. 11/24/2006 1:33:17 PM broa d qr s tach yc a r di a s patients with preexistent BBB during SVT and in patients who, during tachycardia, have AV conduction over an accessory pathway. In the latter situation, marked left-axis deviation can be found during anterograde conduction over a right-sided or posteroseptal accessory bundle and marked right-axis deviation in cases of a left lateral accessory pathway. Configurational Characteristics of the QRS Complex 2 011 77415 I II III V1 Bundle Branch Block–Shaped QRS Complexes An SVT with RBBB aberration is recognized because of a triphasic rSR in lead V1 and a triphasic qRS pattern in lead V6.4,10 In lead V1, the initial r wave reflects normal septal activation, the S wave left ventricular activation, and the R wave delayed activation of the right ventricle. Lead V6 shows a narrow q wave as the result of normal septal activation and an R/S ratio of more than 1. A typical example of RBBB aberration during SVT is shown in Figure 96.4. In VT with an RBBB-like QRS contour, lead V1 usually shows a monophasic or biphasic R wave. The presence of a deep S wave in lead V6 (R : S ratio <1) supports the diagnosis of VT. An R : S ratio <1 in V6 is more common when left axis deviation is present (Fig. 96.8). The differential diagnosis of an LBBB-shaped VT A I II B C 84237 III aVR V6 400 ms FIGURE 96.9. Ventricular tachycardia (left panel) with an LBBB shape showing initial positivity of the QRS in lead V1 (>0.04 second), slurring of the S wave in lead V1 and a distance from the beginning of the QRS to the nadir of the S wave in lead V1 of 140 ms. Lead V6 shows a qR complex. The right panel shows the electrocardiogram during sinus rhythm. and SVT with LBBB aberration is made in lead V1 and V2 and in lead V6. If an R wave is present in either lead V1 or V2, it is small and narrow (<0.04 second) in LBBB aberration, and the down stroke of the S wave is clean and swift (no slurs or notches). Because of the narrow R wave and/or the clean down stroke, the distance from the beginning of the QRS to the nadir of the S wave is 0.07 second or less. In contrast, an R wave of more than 0.04 second, with a slurred down stroke and a delayed S nadir in V1 and/or V2 (>0.07 second) supports the diagnosis of VT.11 A q wave in lead V6 confirms VT (Fig. 96.9). aVL Presence of Q Waves During Tachycardia aVF Coumel and associates9 demonstrated the value of QR complexes during a wide QRS tachycardia as pointing to a ventricular origin for the arrhythmia. This is typically found in VT in patients with a localized ventricular scar because of a previous myocardial infarction. An example is given in Figure 96.8. V1 V2 V3 V4 Duration of the Onset of R to Nadir S in Precordial Leads V5 V6 84258 400 ms FIGURE 96.8. Two types of ventricular tachycardia (VT) in a patient with an old anteroseptal myocardial infarction (C). Both VTs (A,B) have an RBBB shape and clearly show AV dissociation. Note the effect of the frontal plane axis on the R : S ratio in lead V6 in RBBB shaped VT. An R : S <1 is present in the case of a superior axis (B), but R : S >1 with an inferior QRS axis (A). Note also the presence of QR complexes during VT (in III, aVF, V1, and V6 in A, and in V2 and V3 in B), indicating the presence of a scar from a previous myocardial infarction. CAR096.indd 2011 This distance is increased in VT. As pointed out by Brugada et al.,12 the presence of an RS interval of more than 100 ms in one or more precordial leads is highly suggestive of VT. However, such a duration may occur in SVT with AV conduction over an accessory pathway, in SVT with preexistent BBB (especially LBBB), and in SVT during the administration of drugs that slow intraventricular conduction (Fig. 96.6). Table 96.1 lists all the limitations of these different electrocardiographic findings. 11/24/2006 1:33:17 PM 2 012 chapter 96 TABLE 96.1. Limitations of electrocardiographic signs suggestive of a ventricular origin for a wide QRS tachycardia Sign Limitations AV dissociation VA conduction may occur during VT AV junctional rhythm with BBB and AV dissociation Preexistent BBB (especially LBBB) SVT with AV conduction over an accessory pathway Use of drugs slowing intraventricular conduction (class Ia, class Ic, amiodarone) Not helpful in LBBB-shaped QRS SVT with AV conduction over a right-sided or posteroseptal accessory pathway SVT during use of class IC drugs Not helpful in RBBB-shaped QRS Only in VT with localized myocardial scarring or infiltration (sarcoidosis, or amyloidosis) Positive concordancy may occur during SVT with AV conduction over a left posterior accessory pathway SVT on drugs slowing conduction SVT with AV conduction over an accessory pathway Preexistent BBB (especially LBBB) Occurs only at relatively slow VT rates R/O fusion with a contralateral VPC during VT R/O fusion with a ventricular echo beat Requires availability of ECG during sinus rhythm R/O atrial premature beat with aberrant conduction Left-axis deviation (to the left of −30 degrees) Right-axis deviation (to the right of +90 degrees) Presence of q(Q)R complexes in leads other than AVR Concordant pattern in precordial leads R-nadir S >100 ms in one or more intraventricular precordial leads Presence of a supraventricular impulse able to depolarize the ventricles completely (“capture beat”) or partially (fusion complex) Presence of premature beats during sinus rhythm with the same QRS configuration as during wide QRS tachycardia AV, atrioventricular; BBB, bundle branch block; ECG, electrocardiogram; LBBB, left bundle branch block; MI, myocardial infarction; R/O, rule out; SVT, supraventricular tachycardia; VA, ventriculoatrial; VPC, ventricular premature complex; VT, ventricular tachycardia. LBBB Versus RBBB-Like Configuration Localizing the Site of Origin of Ventricular Tachycardia An LBBB-shaped VT indicates that the origin of the arrhythmia is in the right ventricle resulting in delayed activation of the left ventricle. The reverse is true when the site of origin of the VT is in the left ventricle. Then the right ventricle is activated last, resulting in an RBBB-like QRS complex (Fig. 96.10). The ability to treat VT by removing the site of origin, or interrupting the reentrant pathway of the arrhythmia, stresses the necessity to identify (when possible) the site of origin of VT.13 The ECG can be helpful in doing so by looking at the configuration, the width, and the axis (in the frontal and horizontal) plane of the QRS complex of the VT. I II III aVR I aVL aVF V1 III II VT origin right ventricle QRS: LBBB shape I II V2 III aVR V3 aVL I aVF V4 V5 V6 V1 V2 94359b V3 400 msec III VT origin left ventricle QRS: LBBB shape II V4 V5 V6 84237b CAR096.indd 2012 400 msec FIGURE 96.10. Ventricular tachycardia origin and shape of the QRS complex. Left panel: An origin in the right ventricle produces an LBBBlike shape. Right panel: A left ventricular origin gives an RBBB-like QRS configuration. 11/24/2006 1:33:18 PM 2 013 broa d qr s tach yc a r di a s I II III aVR aVL I aVF V1 III FIGURE 96.11. Ventricular tachycardia origin and QRS width. Left panel: An origin close to the interventricular septum results in more simultaneous right and left ventricular activation and therefore a more narrow QRS complex. In contrast (right panel), a VT origin in the lateral ventricular wall results in sequential ventricular activation and a wider QRS complex. V2 I V3 II III V4 II VT origin close to interventriclar septum more simultaneous ventricular activation more narrow QRS. I aVR aVL V5 aVF V1 V6 84237A 400 msec V2 III II V3 VT origin far from interventriclar V4 septum septal ventricular V5 activation wide QRS. V6 The Width of the QRS Complex 94359c 400 msec The QRS Axis When as shown in Figure 96.11, the origin of the VT is close to the interventricular septum, more simultaneous left and right ventricular activation occurs, leading to a more narrow QRS complex. In contrast, a VT origin in the lateral wall of the origin results in sequential ventricular activation and a wider QRS complex. The Frontal Plane As shown in Figure 96.12, a VT origin in the apical part of the ventricle, has a superior axis (to the left of −30 degrees). An inferior axis is present when the VT has an origin in the basal area of the ventricle. I II III aVR aVL I aVF I V1 III II VT origin infero-apical frontal QRS axis II V2 III V3 aVR V4 I aVL V5 aVF V6 V1 400 msec V2 V3 FIGURE 96.12. Ventricular tachycardia origin and QRS axis in the frontal plane. An apical origin results in a superiorly directed axis (left panel). In contrast, a basal origin leads to an inferior QRS axis (right panel). CAR096.indd 2013 III VT origin antero-basal frontal QRS axis II V4 V5 V6 9914a 400 msec 11/24/2006 1:33:18 PM 2 014 chapter A 96 B I I II posterior LV RV III II aVR III aVL aVF aVR aVL posterior V6 V 1 V1 anterior V2 V1 anterior V3 V4 V4 V5 V6 FIGURE 96.13. A concordant pattern in localizing the VT origin in the horizontal plane. Left panel: A VT arising in the apical area of the left ventricle resulting in a negative concordancy of all precordial leads. Right panel: Ventricular activation starts in the posterior area, resulting in positive concordancy of all precordial leads. The latter can be found in left posterior VT but also in SVT with AV conduction over a left posterior accessory AV pathway. RV V2 V3 V6 LV aVF V1 V5 86665a V6 94359a 400 ms The Horizontal Plane As shown in Figure 96.13, when a VT arises in the anteroapical area of the ventricle, all precordial QRS complexes will be negative (negative concordancy). When ventricular activation starts in the left posterior area, all precordial QRS complexes will be positive (positive concordancy). As pointed out before, positive concordancy can also be found when a supraventricular tachycardia with AV conduction over a left posterior accessory pathway is present. The ECG for localizing VT is most reliable when there is little or no cardiac damage. When scar tissue is present in the ventricle (as after myocardial infarction), localizing VT origin by ECG is often difficult, and intracardiac mapping will be necessary especially when catheter ablation of VT is considered (see Chapter 102). from the endocardially located idiopathic VT’s. (See also Chapter 102.) Idiopathic left VTs all have an RBBB-like shape because of an origin in the left ventricle. Figure 96.16 shows three A B I I II II III III aVR aVR Etiology of Ventricular Tachycardia aVL aVL Most VTs have a previous myocardial infarction as their etiology, and a QR complex during VT can be very helpful to make that diagnosis. However, characteristic ECG patterns can also be found in idiopathic VT14 and VT in patients with arrhythmogenic right ventricular dysplasia (ARVD).15 Figure 96.14 shows two patterns of idiopathic VT arising in or close to the outflow tract of the right ventricle. Both have an LBBBlike QRS complex indicating a right ventricular origin. In panel A the frontal QRS axis is +70 and lead I shows a positive QRS complex, indicating an origin of the tachycardia in the lateral part of the outflow tract of the right ventricle. In panel B the frontal QRS axis is inferior and the QRS is negative in lead I pointing to an origin on the septal site in the right ventricular outflow tract. Recently, it has become clear that ventricular tachycardias may originate in the root of the pulmonary artery and the aorta.16–19 In those patients, epicardially located muscle fibers run to the base of the right or left ventricle. An example is given in Figure 96.15. These tachycardias require a different catheter ablative approach aVF aVF V1 V1 V2 V2 V3 V3 V4 V4 V5 V5 V6 V6 CAR096.indd 2014 Free wall RVOT Septal side RVOT FIGURE 96.14. Two patterns of idiopathic VT arising in or close to the outflow tract of the right ventricle. See text. 11/24/2006 1:33:18 PM 2 015 broa d qr s tach yc a r di a s aorta LV RV FIGURE 96.15. Two examples of idiopathic VTs arising in the aortic root. The one on the left has its origin close to the right coronary cusp and is connected by a muscle band to the epicardium of the outflow tract of the right ventricle. The one on the right is originating close to the left coronary cusp and is connected to the posterior part of the left ventricular outflow tract. A I V1 II V2 III V2 III V3 aVR V4 aVL V5 aVF V6 V4 aVL V5 aVF V6 C 01004 II III aVR aVL aVF V1 V2 V3 V4 V5 V6 95165 400 ms FIGURE 96.16. Three types of left ventricular idiopathic VT. See text. CAR096.indd 2015 II aVR B 99325 V1 V3 I 93152a I types. The most common one is shown in panel A. The frontal QRS axis shows left axis deviation. The site of origin of the VT is in or close to the posterior fascicle of the LBB. In panel B, the frontal QRS axis is further leftward (a socalled northwest axis). This tachycardia arises more anteriorly, close to the interventricular septum. The least common idiopathic left VT is the one shown in panel C. Now, the frontal QRS axis is inferiorly directed. This VT originates in the anterior fascicle of the LBB. In ARVD, there are three predilection sites in the right ventricle: the inflow and outflow tracts, and the apex. While the first two sites have a QRS configuration during tachycardia that is difficult to differentiate from right ventricular idiopathic VT, left axis deviation in a young person with an LBBB-shaped VT should immediately lead to the suspicion of ARVD. In fact, there is an important rule in LBBB-shaped VT with left axis deviation that cardiac disease should be suspected and that idiopathic right ventricular VT is extremely unlikely. Figure 96.17 gives an example of an LBBB-shaped VT in a patient with ARVD. The typical ECG features found in ARVD both during VT and during sinus rhythm can be found elsewhere.15 When the broad QRS is identical during tachycardia and sinus rhythm, one has to differentiate SVT with preexistent BBB from bundle branch reentrant tachycardia.20 In diseased hearts, especially when the bundle branches and the interventricular septum are involved, a tachycardia may occur based on a circuit with anterograde conduction down one bundle branch or one of the left-sided fascicles, and, after septal activation, retrograde conduction over another branch 11/24/2006 1:33:19 PM 2 016 chapter A 96 95058 B 85252 I I II II III III aVR aVR aVL aVF V1 V2 V3 aVL aVF V1 V2 V4 V3 V5 V4 V6 85305 400 ms FIGURE 96.17. A VT in a patient with diffuse arrhythmogenic right ventricular dysplasia. (A) A VT with an LBBB-like shape and a frontal QRS axis of −60 degrees. The QRS width is 200 msec. (B) Characteristic ECG fi ndings during sinus rhythm such as T-wave inversion in leads V1 to V3 and a different QRS width in V1 and V2 (120 ms) and V6 (90 ms). V5 V6 MACVU 002C 400 ms FIGURE 96.19. Example of bundle branch reentrant ventricular tachycardia in a patient with a previous anteroseptal myocardial infarction. During VT the impulse goes down over the left anterior fascicle and back up over the right bundle branch. The tachycardia is shortly interrupted by two paced ventricular beats, but resumes immediately after three conducted sinus beats. The sinus beats also show that anterograde conduction to the ventricle went by way of the left anterior fascicle because of anterograde block in the left posterior fascicle and the right bundle branch. of the bundle branch system (Fig. 96.18). Figure 96.19 gives a clinical example in a patient with a previous anteroseptal myocardial infarction. Bundle branch reentry tachycardia may occur in patients with anteroseptal myocardial infarction, idiopathic dilated cardiomyopathy, myotonic dystrophy, after aortic valve surgery, and after severe frontal chest trauma. Value of the ECG During Sinus Rhythm FIGURE 96.18. The tachycardia circuit in bundle branch or fascicular reentrant tachycardia. On top, the situation during sinus rhythm with anterograde block in the right bundle and the left posterior fascicle. During VT the impulse uses either the right bundle branch (bundle branch reentry) or the posterior fascicle (fascicular reentry) for retrograde conduction. CAR096.indd 2016 The ECG during sinus rhythm may show changes such as preexistent BBB, ventricular preexcitation, or an old myocardial infarction, which are very helpful in correctly interpreting the ECG during broad QRS tachycardia. Also, the presence of AV conduction disturbances during sinus rhythm make it very unlikely that a broad QRS tachycardia in that patient has a supraventricular origin, and, as shown in Figure 96.20, a QRS width during tachycardia more narrow than during a sinus rhythm points to a VT. 11/24/2006 1:33:19 PM 2 017 broa d qr s tach yc a r di a s A I II III FIGURE 96.20. Tachycardia QRS smaller than QRS during sinus rhythm. On the left, sinus rhythm is present with a very wide QRS because of an anterolateral myocardial infarction and pronounced delay in left ventricular activation. On the right, a VT arising on the right side of the interventricular septum results in more simultaneous activation of the right and left ventricle than during sinus rhythm and therefore, a smaller QRS complex. aVR aVL V1 It is important not to panic when one is confronted with a wide QRS tachycardia. Statistically, VT is much more common than SVT, also when the tachycardia is hemodynamically well tolerated. The patient should be examined for clinical signs of AV dissociation, and the 12-lead ECG should be systematically evaluated. When the tachycardia is hemodynamically not tolerated, emergent cardioversion should be performed. If the tachycardia is tolerated but the diagnosis is in doubt, the patient should not be treated with adenosine or verapamil; procainamide should be given instead. Summary Most wide QRS tachycardias have a ventricular origin. Correct diagnosis, which includes the identification of underlying heart disease, has important prognostic and therapeutic implications. In ventricular tachycardia, treatment during the arrhythmia depends on the hemodynamic tolerance of the arrhythmia. When underlying heart disease is present, it should be corrected when possible. Currently, implantable cardiodefibrillator (ICD) implantation is often required (see Chapter 98). In some VT patients, cure can be obtained by catheter ablation (see Chapter 102). References 1. 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