Basic and Bedside Electrocardiography, 1st Edition (2009)

Chapter 22. Wide Complex Tachycardia

Causes of Wide Complex Tachycardia

·         Wide complex tachycardia indicates the presence of fast and regular heart rate of >100 beats per minute (bpm) associated with wide QRS complexes measuring at least 120 milliseconds.

·         A wide complex tachycardia can be ventricular or supraventricular.

o    Ventricular tachycardia (VT) has a wide QRS complex because the arrhythmia originates below the bifurcation of the bundle of His. The impulse does not follow the normal atrioventricular (AV) conduction system and activation of the ventricles does not occur simultaneously (Fig. 22.1A).

o    Supraventricular tachycardia (SVT) has narrow QRS complexes because the impulse originates above the bifurcation of the bundle of His. The impulse follows the normal AV conduction system and activation of both ventricles is simultaneous. SVT can have wide QRS complexes when there is:

§  Preexistent bundle branch block (B).

§  AV reciprocating tachycardia (AVRT) due to the presence of a bypass tract. This wide complex tachycardia is also called antidromic AVRT (C).

§  Ventricular aberration or rate related bundle branch block (D).

Figure 22.1: Wide Complex Tachycardia. (A) Ventricular tachycardia. (B-D) Examples of supraventricular (SVT) with wide QRS complexes. (B) SVT with preexistent bundle branch block. (C) Antidromic atrioventricular reciprocating tachycardia from the presence of a bypass tract. (D) SVT is conducted with aberration. (image) indicates the origin of the impulse; (arrows) the direction of the spread of the electrical impulse.

Wide QRS Complex from Ventricular Tachycardia

·         Distinguishing VT from wide complex SVT is always a diagnostic challenge. Unless the patient is unstable, a 12-lead electrocardiogram (ECG) should always be recorded when there is wide complex tachycardia because it provides much more diagnostic information than a single-lead rhythm strip.

·         Single-lead rhythm strip: Very often, the tachycardia is recorded only on a rhythm strip obtained from a cardiac monitor. When only a single-lead ECG is available for interpretation, any of the following findings is diagnostic of VT:

o    Unusually wide QRS complexes (Fig. 22.2).

o    Complete AV dissociation (Fig. 22.3).

o    Ventricular fusion complex (Figs. 22.4,22.5,22.6).

o    Sinus captured complex or Dressler beat (Fig. 22.7).

o    Ventriculoatrial conduction with block (Figs. 22.8 and 22.9).

·         Unusually wide QRS complexes:

o    When the tachycardia has a right bundle branch block (RBBB) configuration, the tachycardia is ventricular if the width of the QRS complex exceeds 0.14 seconds. If the tachycardia has a left bundle branch block (LBBB) configuration, the tachycardia is ventricular if the QRS complex exceeds 0.16 seconds. There should be no preexistent bundle branch block or preexcitation in baseline ECG and the patient should not be taking any antiarrhythmic medication that prolongs intraventricular conduction.

Figure 22.2: Tachycardia with Unusually Wide QRS Complexes. The QRS complexes are unusually wide measuring >160 milliseconds. This run of tachycardia with unusually wide QRS complexes is due to ventricular tachycardia (VT). The first complex (circled) shows no evidence of preexcitation or preexistent bundle branch block. The star indicates a fusion complex, which is also diagnostic of VT.

Figure 22.3: Complete Atrioventricular (AV) Dissociation. When complete AV dissociation is present, the diagnosis of the wide complex tachycardia is ventricular tachycardia. Arrows point to P waves that are completely dissociated from the QRS complexes.

Figure 22.4: Ventricular Fusion Complex. The QRS complex marked by the star is a ventricular fusion complex. Ventricular fusion complexes are usually seen at the beginning or end of ventricular tachycardia (VT).When a ventricular fusion complex is present, the wide complex tachycardia is VT.

Figure 22.5: Ventricular Fusion Complexes. A rhythm strip shows fusion complexes that are marked by stars. The ventricular fusion complexes can assume any configuration other than the configuration of the QRS complexes during normal sinus rhythm or during tachycardia. The presence of a ventricular fusion complex during wide complex tachycardia is diagnostic of ventricular tachycardia.

 

Figure 22.6: Ventricular Fusion Complex. (A) Two separate impulses, ventricular and supraventricular, simultaneously activate the ventricles to cause a ventricular fusion complex. (B) A fusion complex occurs when two separate ventricular impulses activate the ventricles simultaneously. (C) A ventricular fusion complex is not possible with two separate supraventricular impulses because both are obligated to follow the same pathway to the ventricles.

Figure 22.7: Sinus Captured and Ventricular Fusion Complexes. (A) 12-lead electrocardiogram during wide complex tachycardia. Ventricular fusion complexes are marked by the letter F. The fusion complexes are preceded by sinus P waves (arrowheads). A sinus captured complex, also called Dressler's beat, is circled. (B) Lead II rhythm strip from the same patient recorded separately during normal sinus rhythm. The sinus-captured complex recorded in lead II is identical to the QRS complex during sinus rhythm and are both circled for comparison.

Figure 22.8: Wide Complex Tachycardia with 2:1 Ventriculoatrial (V-A) Block. V-A conduction is shown in leads II, III, and aVF. The retrogradely conducted P waves (arrows) occur after every other QRS complex representing 2:1 second-degree V-A block. V-A conduction with intermittent V-A block is diagnostic of ventricular tachycardia.

 

Figure 22.9: Ventriculoatrial (V-A) Wenckebach. Lead II rhythm strip shows 2:1 V-A block and 3:2 V-A Wenckebach (arrows on the left half of the rhythm strip)with gradual prolongation of the R-P interval until a ventricular impulse is not followed by an atrial complex. The presence of intermittent V-A conduction suggests that the origin of the tachycardia is ventricular.

o    Differentiating a wide complex tachycardia as having a RBBB or LBBB configuration may be difficult if only a single-lead monitor strip is available for interpretation (Fig. 22.2). However, an unusually wide QRS complex measuring >0.16 seconds is usually VT, regardless of the configuration of the QRS complex.

Ventricular Tachycardia

·         Complete AV dissociation: When sinus P waves are present and there is no relationship between the P waves and the QRS complexes, complete AV dissociation is present (Fig. 22.3). Complete AV dissociation occurs when two separate pacemakers are present: one capturing the atria and the other the ventricles. During VT, the rate of the ventricles is faster than the rate of the atria; thus, the slower atrial impulse will usually find the ventricles refractory. Complete AV dissociation occurring during a wide complex tachycardia is diagnostic of VT.

·         Ventricular fusion complex: In VT, the sinus impulse may be able to capture the ventricles if the sinus impulse is perfectly timed to occur when the ventricles are not refractory. A ventricular fusion complex may occur if the ventricles are partly activated by the sinus impulse and partly by the VT (Figs. 22.4,22.5,22.6).

Ventricular Fusion Complex

·         Ventricular fusion complex: A ventricular fusion complex results when the ventricles are simultaneously activated by two separate impulses, causing a change in the pattern of ventricular activation. At least one of the impulses should originate from the ventricles. A ventricular fusion complex therefore can occur if one impulse is ventricular and the other supraventricular (Fig. 22.6A). It can also occur if both impulses originate from two different locations in the ventricles (Fig. 22.6B). Two separate supraventricular impulses cannot produce a ventricular fusion complex because both supraventricular impulses are obligated to follow the same conduction pathway on their way to the ventricles and will not alter the pattern of ventricular activation (Fig. 22.6C). Thus, when a ventricular fusion complex occurs during a wide complex tachycardia, the diagnosis is VT. The fusion complex can assume any configuration other than the configuration of the QRS complex during sinus rhythm or during the wide complex tachycardia. Examples of ventricular fusion complexes are shown in Figures 22.2, 22.4, and 22.5.

Sinus Captured Complex

·         Sinus captured complex: In VT, the atrium and ventricles are completely dissociated with the ventricular rate faster than the sinus rate. The sinus impulse is, therefore, unable to capture the ventricles, because the ventricles are almost always refractory on arrival of the sinus impulse to the ventricles. If a properly timed sinus impulse arrives at the ventricles when the ventricles are not refractory, the sinus impulse may be able to capture the ventricles partially (resulting in a fusion complex) or completely (resulting in sinus captured complex). A sinus-captured complex during VT is a narrow QRS complex identical to a normally conducted sinus impulse (Fig. 22.7). Very often, sinus P waves are visible preceding fusion or sinus captured complexes. The presence of a sinus-captured complex during wide complex tachycardia is diagnostic of VT.

·         Ventriculoatrial conduction: Ventriculoatrial (V-A) conduction or conduction of an impulse from ventricles to atria is not commonly seen in the ECG, but has been shown to occur in 50% of patients with VT during electrophysiologic testing. One-to-one V-A conduction can occur during VT, but it can also occur during antidromic or wide complex AVRT. Not generally known as a marker of VT is V-A conduction with block.

·         V-A conduction with block:V-A conduction is better appreciated when recorded in a 12-lead ECG rather than a rhythm strip. The retrograde P waves are best recognized in leads II, III, and aVF. Figure 22.8 shows 2:1 V-A block and Figure 22.9 shows V-A Wenckebach. V-A block is not possible when there is antidromic AVRT because the tachycardia will not be able to sustain itself and will terminate if the impulse is blocked (see Chapter 16, Supraventricular Tachycardia due to Reentry). The presence of V-A conduction with intermittent block points to the ventricles as the origin of the arrhythmia and is diagnostic of VT.

Figure 22.10: Wide Complex Tachycardia. When only a rhythm strip is recorded, the following electrocardiogram findings are diagnostic of ventricular tachycardia. (1) Unusually wide QRS complexes measuring >0.16 seconds. (2) Complete atrioventricular dissociation. (3) Ventricular fusion complex (arrow). (4) Sinus captured complex (arrow). (5) V-A Wenckebach (6) Two to one V-A block. The stars mark the sinus P waves. V-A, Ventriculoatrial.

·         The diagrams in Fig. 22.10 summarize the ECG findings of VT when only a rhythm strip is recorded.

The 12-Lead ECG

·         Twelve-lead ECG: A full 12-lead ECG provides more useful information than a single-lead rhythm strip in differentiating VT from wide complex SVT and should always be recorded unless the patient is hemodynamically unstable requiring immediate electrical cardioversion. When a wide complex tachycardia is recorded in a 12-lead ECG, it does not only provide more information; a more organized approach to distinguish VT from wide complex SVT can be used (Fig. 22.11).

·         If a 12-lead ECG is recorded during a wide complex tachycardia, the following algorithm proposed by Brugada et al. attempts to diagnose VT in four simple steps (Fig. 22.11).

Figure 22.11: Algorithm for Wide Complex Tachycardia. (Modified from Brugada et al.)

o    Step 1: Look for an RS complex in V1 to V6. If there is no RS complex, the diagnosis is VT and no further analysis is needed. If an RS complex is present, proceed to step 2.

o    Step 2:Measure the RS duration. If the RS duration is >100 milliseconds, the diagnosis is VT and no further analysis is needed. If the RS duration is ≤100 milliseconds, proceed to step 3.

o    Step 3: Look for AV dissociation. If there is AV dissociation, the diagnosis is VT and no further analysis is needed. If AV dissociation is not present, proceed to step 4.

o    Step 4: The morphologic criteria are used to diagnose VT (Figure 22.11)

§  If the QRS complex is positive in V1, the morphologic criteria for RBBB are used to diagnose VT.

§  If the QRS complex is negative in V1, the morphologic criteria for LBBB are used to diagnose VT.

·         The full algorithm is shown in Figure 22.11. If the diagnosis of VT is not possible after going through these four simple steps, the patient should be further evaluated for other signs of VT using all possible diagnostic modalities including history, physical examination, previous ECG if available, response to vagal maneuvers, and certain pharmacologic agents.

·         If the diagnosis of VT cannot be confirmed, the ECG should be evaluated for wide complex SVT. If the diagnosis remains uncertain after careful evaluation of the wide complex tachycardia, practice guidelines recommend that the tachycardia should be managed as VT.

Step I: Absence of RS Complex in the Precordial Leads is VT

·         The following illustrations will demonstrate step by step how to diagnose VT using the algorithm.

·         Step I: Look for an RS complex in the precordial leads. The first step is to look for RS complex in V1 to V6. Examples of RS complexes are shown in Figure 22.12.

o    If RS complex is not present in any precordial lead V1 to V6, the diagnosis is VT and no further analysis is necessary (Fig. 22.13).

o    If RS complex is present in any of the precordial leads, the diagnosis of VT cannot be confirmed, proceed to step II.

Step II: RS Duration >100 Milliseconds is VT

·         Step II: Measure the RS duration. If an RS complex is present in any precordial lead, the diagnosis of VT is not possible. The next step is to measure the duration of the RS complex. If several RS complexes are present, the RS complex with the widest duration is selected.

o    The duration of the RS complex is measured from the beginning of the R wave to the nadir or lowest point of the S wave as shown in Figure 22.14.

o    If the duration of the RS complex is >100 milliseconds as shown in Figure 22.15, the diagnosis is VT and no further analysis is necessary.

o    If the duration of the RS complex is <100 milliseconds, the diagnosis of VT cannot be confirmed, proceed to step III.

·         A wide complex tachycardia is shown in Figure 22.16. The algorithm is applied to look for VT.

o    Step I: Look for an RS complex. RS complexes are present in V2 to V5. The diagnosis of VT cannot be confirmed.

o    Step II: Measure the duration of the RS complex. V2 is selected because it has the widest RS duration. The duration of the RS complex is >100 milliseconds. The diagnosis is VT and no further analysis is needed.

Step III: AV Dissociation is Diagnostic of VT

·         Step III: Look for AV dissociation. If VT is not diagnosed after steps I and II, the algorithm continues to step III. Step III of the algorithm is to look for AV dissociation.

o    Any of the 12 leads can be used when looking for AV dissociation. If AV dissociation is present, as shown in Figure 22.17, the diagnosis is VT and no further analysis is needed.

o    If AV dissociation is not present, the diagnosis of VT cannot be confirmed, proceed to step IV.

Step IV: Morphologic Criteria

·         Step IV: Morphologic criteria. In the fourth and final step, the QRS complex is classified as having either RBBB or LBBB morphology.

o    The morphology is RBBB if in V1: the QRS complex is positive or the R wave is taller than the S wave.

o    The morphology is LBBB if in V1: the QRS complex is negative or the S wave is deeper than the height of the R wave.

·         RBBB morphology: If the tachycardia has a RBBB morphology, V1 and V6 should be examined for VT.

o    V1: The following findings in V1 favor VT. Monophasic or biphasic QRS complex. Examples of monophasic and biphasic QRS complexes in V1 are shown in Figure 22.18.

o    V6: The following findings in V6 favor VT. Any q wave (except “qrs”), monophasic R wave, r/S ratio <1 (r wave smaller than S wave). These changes are shown in Figure 22.18.

·         If a monophasic or biphasic QRS pattern is present in V1 + any of the described QRS pattern is present in V6, the diagnosis is VT. If the pattern is present only in V1, but not in V6, or the pattern is present only in V6, but not V1, the diagnosis of VT is not possible.

Step IV: Wide Complex Tachycardia with RBBB Morphology

·         The following example (Fig. 22.19) shows how to use the algorithm when there is a wide complex tachycardia with a RBBB configuration.

o    Step I, step II, and step III of the algorithm are unable to make a diagnosis of VT.

Figure 22.12: RS Complexes. Examples of RS complexes are shown diagrammatically. Any complex starting with a q wave or a complex with RSR′ configuration is not an RS complex.

Figure 22.13: Applying the Algorithm. Step I: Look for an RS complex in V1 to V6 only. A qR configuration is seen in V1, V2, V3, V4, V5, and V6. Because there is no RS complex in any of the precordial leads, the diagnosis is ventricular tachycardia. No further analysis is necessary.

Figure 22.14: RS Complexes. Examples of RS complexes are shown. The duration of the RS complex is measured from the beginning of the R wave to the nadir of the S wave.

Figure 22.15: Duration of the RS Complex. The duration of the RS complex is measured from the beginning of the R wave to the lowest portion of the S wave as shown by the arrows. One small block in the electrocardiogram is equivalent to 40 milliseconds and 2.5 small blocks is equivalent to 100 milliseconds. If the RS duration is >100 milliseconds, the diagnosis is ventricular tachycardia and no further analysis is needed. ms, milliseconds.

 

Figure 22.16: Step II: Measure the Duration of the RS Complex. Step I: Look for an RS complex in the precordial leads. RS complexes are seen in V2, V3, V4, V5, and probably V6. Because RS complexes are present, the diagnosis of ventricular tachycardia (VT) cannot be confirmed. Step II: The duration of the RS complex is measured. V2 has the widest RS duration and is magnified to show how the RS is measured. The RS measures 120 milliseconds. The diagnosis is VT and no further analysis is needed. ms, milliseconds.

Figure 22.17: Step III: Look for Atrioventricular (AV) Dissociation. Step I: Look for an RS complex. Because an RS complex is present in V1, V2, and V3, the diagnosis of ventricular tachycardia (VT) can not be confirmed. Step II:Measure the duration of the RS complex. The RS duration in V2 and in V3 is <100 milliseconds. Because the duration of the RS complex is <100 milliseconds, diagnosis of VT can not be confirmed. Step III: Look for AV dissociation. (B)This is the same lead II rhythm strip shown in (A) and is magnified to show the AV dissociation. The P waves (arrows) are completely dissociated from the QRS complexes. When complete AV dissociation is present, the diagnosis is VT and no further analysis is necessary. ms, milliseconds.

 

Figure 22.18: Morphologic Criteria for Right Bundle Branch Block Pattern. Themorphology of the QRS complexes that favor ventricular tachycardia (VT) is shown for V1 and for V6. If a monophasic or biphasic complex is present in V1and any of these QRS patterns is also present in V6, the diagnosis is VT.

Figure 22.19: Wide Complex Tachycardia with Right Bundle Branch Block (RBBB) Morphology. Step 1: Look for an RS complex. RS is present in V6. Step 2: Measure the RS duration. V6 is magnified to show that the RS duration is <100 milliseconds. Step 3: Look for atrioventricular (AV) dissociation. AV dissociation is not present. Step 4:Morphologic criteria. Because V1 is positive with a tall R wave, the morphologic criteria for RBBB are used. In V1, the QRS morphology is biphasic (QR pattern), which favors ventricular tachycardia (VT). In V6, the RS ratio is <1 (r smaller than S). This also favors VT. V1 and V6 match the morphologic criteria for VT; therefore, the diagnosis is VT. ms, milliseconds.

Figure 22.20: Morphologic Criteria for Left Bundle Branch Block (LBBB) Configuration. The diagnosis is ventricular tachycardia if any of the above QRS morphology is present in V1 or V2 and any Q wave is present in V6.When the tachycardia has a LBBB morphology, it is faster and simpler to check V6 first for any Q wave before matching the finding in V1 because the only criterion in V6 is to look for a Q wave.

 

o    Step IV of the algorithm shows RBBB configuration; thus, the RBBB morphologic criteria are used as shown in Figure 22.18.

Step IV: Wide Complex Tachycardia with LBBB Morphology

·         LBBB Morphology: When the wide complex tachycardia has a LBBB configuration, V1 or V2 can be used. This is unlike wide complex tachycardia with RBBB configuration, where only lead V1 is used. The diagnosis is VT if any of the following findings is present in V1 or V2 and also in V6 (Fig. 22.20):

o    V1 or V2:

§  R wave duration in V1 or V2 is ≥0.04 seconds or 40 milliseconds

§  RS duration in V1 or V2 is ≥0.07 seconds or 70 milliseconds

§  Slurring or notching of the downslope of the S wave.

o    V6: Any q wave in V6 will favor VT (Fig. 22.20). This may be a qR, qr, QS, or QRS.

·         If any of these QRS morphologies is present in V1 or V2 + any of the QRS morphologies is present in V6, the diagnosis is VT. If the QRS morphology is present only in V1 or V2, but not in V6, or the QRS morphology is present only in V6g, but not in V1 or V2, the diagnosis of VT is not possible.

Figure 22.21: Applying the Algorithm. Step IV: Steps I, II, and III of the algorithm are unable to diagnose ventricular tachycardia (VT). Step IV: Because the QRS complex in V1 is negative or the S wave is deeper than the R wave, the morphologic criteria for left bundle branch block are used. V6 starts with a q wave. This favors VT. V1 has RS duration of 0.07 seconds. There is also notching of the downslope of the S wave in V2 (bold arrow). Either of these findings favors VT. V1-2and V6 match the morphologic criteria for VT; therefore, the diagnosis is VT.

·         When the tachycardia has LBBB morphology, it is simpler to evaluate V6 before V1 because the only criterion in V6 is simply to look for any “q” wave. If a q wave is not present, the diagnosis of VT is not possible. If the tachycardia has RBBB morphology, V1 should be inspected first because the only criterion in V1 is to look for a monophasic or biphasic complex.

·         The ECG in Figure 22.21 shows a wide complex tachycardia with LBBB morphology (rS complex is present in V1). Steps I to III of the algorithm are unable to make a diagnosis of VT. Using step IV of the algorithm, the QRS complex has a LBBB configuration; thus, the morphologic criteria for LBBB are used (see Figure 22.21).

Other Findings Diagnostic of VT

·         Other findings: If VT cannot be diagnosed after going through the algorithm, there are other ECG findings not included in the algorithm that may suggest VT.

o    RBBB morphology with left axis deviation >-30° (Fig. 22.22).

o    LBBB morphology with right axis deviation >+90° (Fig. 22.23).

Figure 22.22: Right Bundle Branch Block with Left Axis Deviation. This finding favors ventricular tachycardia.

o    Northwest axis: The QRS axis is between -90° to -180° (Fig. 22.24).

o    Concordant QRS complexes: All QRS complexes in V1 to V6 are similar and are all pointing upward (positive concordance) or downward (negative concordance), as shown inFigures 22.24 and 22.25.

o    Previous ECG: A previous ECG shows myocardial infarction (Fig. 22.26) or previous ECG shows that during sinus rhythm, bifascicular block is present, which changes in configuration during tachycardia (Fig. 22.27).

·         Concordance: Negative concordance implies that all QRS complexes in the chest leads are pointing downward. Positive concordance implies that all the QRS complexes are pointing upward (Figs. 22.24 and 22.25).

·         Previous ECG: If myocardial infarction is present in a previous ECG, the wide complex tachycardia is VT. This is based on the observation that VT is frequently associated with structural cardiac disease especially when there is left ventricular dysfunction (Fig. 22.26).

Figure 22.23: Left Bundle Branch Block with Right Axis >90°. This finding usually indicates ventricular tachycardia (VT). Note also the presence of complete AV dissociation (arrows), which also indicates VT.

·         Previous ECG: If LBBB or a preexistent bifascicular block such as RBBB plus a fascicular block is present in a previous ECG and the morphology of the QRS complex changes during the tachycardia, the diagnosis is VT (Fig. 22.27). This is based on the assumption that ventricular aberration cannot occur when only one fascicle is intact.

Findings Favoring SVT

·         Wide complex SVT: After evaluating the ECG for VT and the diagnosis of VT cannot be confirmed, the following findings in the 12-lead ECG suggest that the wide complex tachycardia is supraventricular.

o    Triphasic pattern in V1 and in V6: SVT with RBBB configuration has a triphasic rSR′ pattern in V1 and a triphasic qRS pattern in V6 as shown in Figure 22.28. This is diagnostic of SVT.

Figure 22.24: Concordance and Northwest Axis. There is negative concordance of the QRS complexes in the precordial leads (all QRS complexes in V1-V6 are pointing downward with a left bundle branch block configuration). Additionally, the axis of the QRS complex is between -90° and -180° (northwest axis). Any of these findings indicates ventricular tachycardia.

o    Rabbit's ear: In V1, if the QRS complex has rabbit ear sign (left ear taller than right ear) or Rr′ configuration, the diagnosis is usually VT (Fig. 22.29). If the configuration is rR7foot; (right ear taller than left), the finding is not helpful but could be SVT if V6 is triphasic (qRs) or R/S ratio is >1 (R wave taller than S wave).

o    Previous ECG: The diagnosis is SVT if a previous ECG shows preexistent bundle branch block and the QRS complexes are identical during tachycardia and during normal sinus rhythm (Figs. 22.30 and 22.31). The presence of preexcitation in baseline ECG also suggests that the wide complex tachycardia is supraventricular (Fig. 22.32).

o    Preexistent RBBB. If a previous ECG shows preexistent RBBB and the QRS pattern during sinus rhythm is identical to the QRS complexes during tachycardia, the tachycardia is supraventricular (Fig. 22.30).

Figure 22.25: Concordant Pattern. There is positive concordance of all QRS complexes from V1 to V6 (all QRS complexes are pointing up in V1-V6). Positive concordance with a right bundle branch block configuration during a wide complex tachycardia is usually ventricular tachycardia although a wide complex SVT due to antidromic AVRT is also possible (see Fig. 22.32).

o    Preexistent LBBB: A similar example of wide complex SVT from preexistent LBBB is shown (Fig. 22.31). The configuration of the QRS complexes is the same during tachycardia and during normal sinus rhythm.

o    Preexcitation: When preexcitation is present during normal sinus rhythm, the wide complex tachycardia is almost always the result of antidromic AVRT. Very often, the QRS complex during tachycardia is similar to the QRS complex during normal sinus rhythm (Fig. 22.32).

Other Useful Modalities

·         In addition to the 12-lead ECG, the following modalities are helpful in the diagnosis of wide complex tachycardia.

o    History: The history is often more important than the ECG in differentiating VT from SVT. The most important feature in the history that will favor VT is the presence of a previous MI.

Figure 22.26: Previous Myocardial Infarction. (A) A wide complex tachycardia. (B) A 12-lead electrocardiogram (ECG) obtained from the same patient during normal sinus rhythm. QS complexes with elevated ST segments are present in V2-4. There are also pathologic Q waves in leads II, III, and aVF consistent with anterior and inferior myocardial infarctions (MI).When a previous MI is present by history or by ECG, a wide complex tachycardia occurring after the MI favors ventricular tachycardia.

Figure 22.27: Previous Left Bundle Branch Block (LBBB). (A) Normal sinus rhythm with LBBB.When a wide complex tachycardia occurs in a patient with preexistent LBBB and the configuration of the QRS complex changes during tachycardia (B), the diagnosis is ventricular tachycardia. This is based on the assumption that when there is bifascicular block, the impulse is obligated to follow the only remaining fascicle, thus ventricular aberration as a cause of the tachycardia is not possible.

 

Figure 22.28: Wide Complex Supraventricular Tachycardia (SVT). Triphasic rSR′ pattern in V1 combined with triphasic qRS pattern in V6 favor the diagnosis of SVT.

§  If the patient had a previous MI and the tachycardia occurred after the MI, the diagnosis is VT.

§  If the patient has history of tachycardia and has preexcitation, the diagnosis is SVT.

o    Physical examination: The presence of hemodynamic instability does not differentiate ventricular from supraventricular tachycardia with a wide QRS complex. The following physical findings however are diagnostic of VT.

§  Cannon “A” waves

§  Varying intensity of the first heart sound

§  Varying volume of the arterial pulse

Figure 22.29: Wide Complex Supraventricular Tachycardia (SVT). (A) When lead V1 shows Rr′ (left rabbit's ear taller than right rabbit's ear), the pattern favors ventricular tachycardia. (B) If lead V1 shows rR′ (also called right rabbit ear taller than left rabbit ear), the finding is not specific but could be SVT if V6 is triphasic (qRS) or the R wave is taller than S wave (R/S ratio >1).

Figure 22.30: Wide Complex Supraventricular Tachycardia (SVT) from Preexistent Right Bundle Branch Block (RBBB).Electrocardiogram (A) and (B) are from the same patient. Note that the configuration of the QRS complexes during normal sinus rhythm (A) is identical to the QRS complexes during tachycardia (B) because of preexistent RBBB.

o    Vagal stimulation: If the wide complex tachycardia is due to SVT, vagal stimulation may terminate the arrhythmia or may cause significant slowing of the heart rate. This will allow the arrhythmia to be diagnosed more appropriately (Fig. 22.33). The rhythm should be recorded during vagal stimulation.

o    Pharmacologic agents: Adenosine, a short-acting AV nodal blocker, is useful in terminating wide complex SVT that are AV nodal-dependent. The tachycardia should be recorded while adenosine is being injected. The cause of the tachycardia may be identified even if the tachycardia does not respond to adenosine (Fig. 22.34).

Figure 22.31: Wide Complex Supraventricular Tachycardia (SVT) from Preexistent Left Bundle Branch Block (LBBB).Electrocardiogram (A) and (B) are from the same patient. Figure (A) shows the patient during normal sinus rhythm and (B) during tachycardia. Note that the configuration of the QRS complexes during the tachycardia (B) is the same as during normal sinus rhythm (A) consistent with SVT with preexistent LBBB.

Figure 22.32: Wide Complex Supraventricular Tachycardia (SVT) from a Bypass Tract. (A) Normal sinus rhythm with short PR interval and delta waves (arrows) from preexcitation. (B) From the same patient during wide complex tachycardia. The presence of preexcitation in baseline electrocardiogram suggests that the wide complex tachycardia is due to antidromic atrioventricular reciprocating tachycardia.

 

Figure 22.33: Wide Complex Tachycardia from Atrial Flutter. Carotid sinus stimulation can slow the ventricular rate transiently resulting in lengthening of the R-R intervals. This will allow the baseline to be inspected for atrial activity. Atrial flutter waves can be demonstrated during transient lengthening of the R-R interval (arrows). The tachycardia is due to atrial flutter and the wide QRS complexes are due to preexistent bundle branch block.

·         If the diagnosis of the wide complex tachycardia remains uncertain after careful evaluation of all available clinical information, practice guidelines recommend that the patient should be treated as VT.

Pharmacologic Agents

·         Figure 22.34 shows a wide complex tachycardia from SVT diagnosed with injection of adenosine, a shortacting AV nodal blocker. It should be given only if the wide complex SVT is known to be supraventricular in origin. It should not be given if the diagnosis is uncertain. It is also helpful in identifying the mechanisms of other types of wide complex tachycardia by slowing the heart rate, as shown in Figure 22.34B.

Figure 22.34: Wide Complex Tachycardia and Intravenous Adenosine. (A) Twelve-lead electrocardiogram showing a wide complex tachycardia. (B) Leads I, II, and III were recorded while adenosine was being injected intravenously. Although the ventricular rate slowed significantly, the configuration of the QRS complexes remained unchanged because of preexistent bundle branch block. Arrows point to the presence of atrial tachycardia with a rate of 167 beats per minute. The atrial rate is the same as the rate of the wide complex tachycardia.

Wide Complex Tachycardia

Summary of ECG Findings

·         VT: Any of the following ECG findings suggests VT:

o    Complete AV dissociation

o    Ventricular fusion complex

o    Sinus captured complex

o    Ventriculoatrial conduction with second degree block

o    Wide QRS complexes measuring >140 milliseconds when the tachycardia has a RBBB pattern or >160 milliseconds when the tachycardia has a LBBB pattern. This observation is not helpful if there is preexistent bundle branch block, preexcitation, or the patient is taking antiarrhythmic medications that prolong intraventricular conduction such as type IA or IC agents.

o    If there is no RS complex in the precordial leads.

o    If RS complex is present in the precordial leads and the RS duration measures >100 milliseconds.

o    If the QRS complex in V1 has RBBB configuration that is monophasic or biphasic and the configuration in V6 is qR, QS, monophasic R wave or rS (R/S <1).

o    When there is LBBB morphology with right axis deviation >+90° or >-60°.

o    When there is RBBB morphology with left axis deviation <-30°.

o    If the axis of the QRS complex is between -90° and -180° also called northwest axis.

o    When QRS complexes are concordant in the precordial leads:

§  LBBB morphology: When the QRS complexes in the precordial leads are negatively concordant with LBBB morphology, this is almost always from VT.

§  RBBB morphology: When the QRS complexes are positively concordant with RBBB morphology, this is usually VT although wide complex SVT from antidromic AVRT is also possible.

o    If a previous 12-lead ECG is available, the diagnosis is VT if:

§  A previous myocardial infarction (MI) is present.

§  Bifascicular block is present during normal sinus rhythm (LBBB or RBBB +a fascicular block) and the QRS morphology becomes different during the tachycardia.

·         SVT: Any of the following ECG findings is consistent with SVT:

o    The tachycardia has RBBB configuration with a triphasic rSR′ pattern in V1 and a triphasic qRS pattern in V6.

o    In V1, right rabbit ear is taller than left. In V6, there is a triphasic QRS complex or R wave is taller than S wave (R/S ratio >1).

o    When a previous 12-lead ECG is available, the diagnosis is SVT if:

§  Bundle branch block is present during normal sinus rhythm and the QRS configuration is identical during tachycardia (wide complex SVT from preexistent bundle branch block).

§  Preexcitation or Wolff-Parkinson-White (WPW) ECG is present during normal sinus rhythm (antidromic AVRT).

Mechanism

·         Complete AV dissociation: In VT, the ventricles are driven by an impulse that is faster and separate from that of the atria. Generally, the atria continue to be controlled by normal sinus rhythm, which has a slower rate and is independent from the ectopic activity occurring in the ventricles. The presence of two independent pacemakers, one controlling the atria and the other the ventricles, will result in complete AV dissociation.

·         Wide QRS complexes: Ventricular tachycardia has wide QRS complex because the ventricles are driven by an impulse occurring below the bifurcation of the bundle of His. Thus, the ventricles are not activated simultaneously because the impulse has to spread from one ventricle to the other ventricle outside the normal conduction system. This causes the QRS complexes to be wide measuring ≥120 milliseconds.

·         Absence of RS complex in the precordial leads: Absence of RS complex in the precordial leads indicates VT. When this occurs, the QRS complex usually starts with a q wave. The q waves indicate that the ectopic ventricular impulse originates from the epicardium and spreads from epicardium to endocardium, causing q waves in the precordial leads. This is in contrast to SVT, which usually activates the ventricles through the His-Purkinje system and therefore the spread of the ventricular impulse is from endocardium to epicardium, causing an RS complex to be inscribed in at least one of the precordial leads.

·         Wide RS interval: The RS interval, measured from the beginning of the R wave to the lowest point of the S wave is equivalent to the spread of the impulse across the thickness of the myocardium. If the RS interval exceeds 100 milliseconds, the diagnosis is VT. This is based on the assumption that in VT, activation of the ventricles will be less efficient and will take longer because the impulse is propagated by muscle cell to muscle cell conduction, as opposed to SVT where activation of the myocardium will be faster because the impulse is conducted through the more efficient His-Purkinje system.

·         Fusion and sinus captured complexes: Although the atrial rate or the rate of the sinus impulse is slower than the rate of the ventricles during VT, a properly timed sinus impulse may arrive at the ventricles when the ventricles are not refractory and may be able to capture the ventricles partially (resulting in fusion complexes) or completely (resulting in sinus captured beats). Thus, when fusion or sinus captured complexes are present, the diagnosis is VT.

·         V-A conduction:When there is VT, the ventricular impulse may be conducted to the atria retrogradely across the AV node, causing the atria to be activated from below upward. This will result in inverted P waves in leads II, III, and aVF. V-A conduction is not uncommon during VT. Wellens et al. showed that in 70 patients with VT, approximately 50% had V-A conduction during electrophysiologic testing, with 23 having 1:1 V-A conduction, 7 having 2:1 V-A, conduction, and 2 having V-A Wenckebach. V-A block may occur spontaneously. It could also be induced by carotid sinus pressure. One to one V-A conduction is not diagnostic of VT because this can also occur in wide complex AVRT. However, intermittent V-A conduction from V-A block is diagnostic of VT. V-A block is not generally known as a marker of VT because V-A conduction is not commonly seen in the surface ECG.

Clinical Findings

·         Other modalities that are useful in differentiating VT from wide complex SVT: Although the 12-lead ECG serves as the foundation for differentiating VT from wide complex SVT, there are other modalities that are also useful. These include the history, physical examination, response to carotid sinus pressure, and other vagal maneuvers.

o    Clinical presentation: The hemodynamic condition of the patient is not reliable in distinguishing VT from SVT. A patient presenting with hypotension, dizziness, or syncope does not necessarily imply that the tachycardia is ventricular. Conversely, a patient who is hemodynamically stable during the tachycardia does not necessarily indicate that the tachycardia is supraventricular. When the heart rate is very rapid (usually ≥150 beats per minute), patients usually become symptomatic and even patients with SVT may become hemodynamically unstable when there is associated left ventricular systolic or diastolic dysfunction.

o    History: The history is often more important than the ECG in differentiating VT from wide complex SVT.

§  History of previous MI favors VT. The tachycardia should occur after (not before) the onset of the MI.

§  History of preexcitation (WPW syndrome) indicates wide complex SVT.

o    Physical examination: The following physical findings suggest VT. The findings are based on the presence of AV dissociation, which is very specific for VT.

§  Cannon “A” waves in the neck veins:When atrial and ventricular contractions are completely dissociated, simultaneous contraction of the atria and ventricles may occur intermittently. When atrial contraction is simultaneous with ventricular contraction, cannon “A” waves will appear in the neck representing contraction of the atria against a closed tricuspid valve. This is manifested as intermittent prominent pulsations in the neck veins.

§  Varying intensity of the first heart sound. Another sign of AV dissociation is varying intensity of the first heart sound. The mechanism for the varying intensity of the first heart sound has been previously discussed in Chapter 8, Atrioventricular Block. The first heart sound is due to closure of the AV valves and the intensity depends on the position of the valves at the onset of systole. If the AV valves are widely open when systole occurs, the first heart sound will be loud. If the AV valves are almost closed at the onset of systole, the first heart sound will be very soft. Because the atrial kick (P wave) pushes the AV valves away from their coaptation points, a short PR interval will cause the ventricles to contract immediately when the AV valves are widely open, which will result in a loud first heart sound. If the PR interval is unusually prolonged, the AV valves will float back to a semiclosed position before the onset of ventricular contraction; thus, the first heart sound will be softer. Because AV dissociation is associated with varying PR intervals, the position of the AV valves at the onset of systole will be variable; hence, the intensity of the first heart sound will also be variable.

§  Varying pulse volume: If atrial contraction is perfectly timed to occur just before ventricular contraction, ventricular filling is augmented and a larger volume is ejected. Because the PR interval is variable when there is AV dissociation, atrial contribution to left ventricular filling will vary resulting in varying pulse volume.

o    Carotid sinus pressure and other vagal maneuvers: Another method of distinguishing VT from SVT is to perform vagal maneuvers including carotid sinus pressure. These procedures may terminate wide complex SVT, but not VT.

Acute Therapy

·         Immediate therapy depends on the clinical presentation of the patient.

o    Unstable patient: If the patient is unstable with hypotension or gross heart failure or the patient is having symptoms of severe ischemia related to the tachycardia, electrical cardioversion is indicated whether the wide complex tachycardia is ventricular or supraventricular.

o    Stable patient: If the patient is stable, pharmacologic therapy can be used. Elective cardioversion is also an option in stable patients if the tachycardia is due to VT or there is uncertainty about the etiology of the wide complex tachycardia. Carotid sinus stimulation and other vagal maneuvers are also helpful and should be tried initially to terminate SVT. It is also helpful in distinguishing VT from wide complex SVT.

·         Pharmacologic therapy: Among stable patients, the type of pharmacologic agent will depend on whether the tachycardia is known to be ventricular, supraventricular, or the etiology of the wide complex tachycardia remains uncertain.

o    Wide complex tachycardia due to SVT: The treatment for wide complex SVT is similar to the treatment of narrow complex SVT. Carotid sinus pressure may terminate the arrhythmia and should be attempted before intravenous medications are given. If the arrhythmia cannot be terminated with vagal maneuvers, the drug of choice is adenosine given intravenously. If adenosine is not effective, another AV nodal blocker may be given. The choice of the AV nodal blocking agent will depend on the presence or absence of LV dysfunction as described under the treatment of narrow complex SVT.

§  Wide complex tachycardia due to antidromic AVRT: If the wide complex SVT is due to antidromic AVRT (WPW syndrome), the AV node may not be part of the reentrant circuit (see the Wide Complex or Antidromic AVRT section in Chapter 20, Wolff-Parkinson-White Syndrome). In antidromic AVRT, anterograde conduction of the atrial impulse occurs at the bypass tract and retrograde conduction from ventricle to atrium may occur through another bypass tract instead of the AV node especially when there is Ebstein's anomaly. Thus, the use of AV nodal blockers will not be effective because the AV node is not part of the reentrant circuit. Type IA, type IC, and type III antiarrhythmic agents that will block conduction through the bypass tract are effective agents in terminating the tachycardia. Procainamide, ibutilide, and flecainide are the preferred agents.

§  The intravenous administration of calcium channel blockers, beta blockers, or adenosine may not be appropriate unless the tachycardia is definitely SVT because these pharmacologic agents are not only ineffective, but may also cause hemodynamic instability or even death if the wide complex tachycardia turns out to be VT.

o    Wide complex tachycardia from VT: If the wide complex tachycardia has been shown to be ventricular in origin, the acute treatment is similar to monomorphic VT. The choice of antiarrhythmic agent will depend on the presence or absence of heart failure or left ventricular dysfunction as discussed in Chapter 21, Ventricular Arrhythmias. For stable patients, procainamide and sotalol are preferred agents, although amiodarone is also acceptable and becomes the preferred agent when there is left ventricular dysfunction or heart failure.

o    Diagnosis uncertain: If the diagnosis of the wide complex tachycardia remains uncertain, calcium channel blockers, beta blockers, or other agents for terminating SVT should not be tried because these agents can cause hemodynamic instability, especially when there is left ventricular dysfunction. In patients who are hemodynamically unstable, electrical cardioversion with appropriate sedation is recommended (Class I). In stable patients, the preferred agents are either procainamide or amiodarone because both agents are effective for VT or SVT. Intravenous procainamide is recommended as initial therapy in stable patients. Intravenous amiodarone is recommended in patients who are hemodynamically unstable, refractory to electrical cardioversion, or if the arrhythmia is recurrent in spite of IV procainamide. Lidocaine is reserved for wide complex tachycardia in patients with poor left ventricular function associated with acute MI or myocardial ischemia. Electrical cardioversion is also an option even if the patient is hemodynamically stable or if the patient does not respond to the chosen antiarrhythmic medication (Table 22.1).

 

 TABLE 22.1 Acute Management of Wide Complex Tachycardia of Uncertain Diagnosis According  to the ACC/AHA/ESC Practice Guidelines in the Management of Patients with Supraventricular  Arrhythmias

 Clinical

Recommendation

Level of Recommendation

 

 Unstable patients

DC electrical cardioversion

Class I

 

 Stable patients

Procainamide

Class I

 
 

Sotalol

Class I

 
 

Amiodarone

Class I

 
 

DC cardioversion

Class I

 
 

Lidocaine

Class IIb

 
 

Adenosine

Class IIb

 
 

Beta blockers

Class III

 
 

Verapamil

Class III

 

 Patients with poor LV function

Amiodarone

Class I

 

DC cardioversion

Class I

 
 

Lidocaine

   

 All pharmacologic agents are given intravenously.

 

 ACC, American College of Cardiology; AHA, American Heart Association; ESC, European Society of

 

 Cardiology; LV, left ventricular; DC, direct current.

 
         

 

·  Electrolyte abnormalities, myocardial ischemia, blood gas, and other metabolic disorders should be identified and corrected. Medications that may be proarrhythmic should be eliminated.

Prognosis

·         Prognosis for VT is worse than SVT. Sustained VT is usually associated with structural cardiac disease such as acute myocardial infarction, cardiomyopathy, or other myocardial diseases resulting in impaired systolic function. The presence of ventricular tachycardia in this setting is associated with a high mortality. These patients are candidates for implantation of automatic implantable defibrillator. Overall prognosis depends on the underlying cardiac disease and severity of left ventricular dysfunction.

·         If the wide complex tachycardia is due to SVT, prognosis is the same as for narrow complex SVT.

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