Ventricular Tachycardia

Melanie Maytin

Bruce A. Koplan

Introduction

Ventricular tachycardia (VT) is defined as a wide QRS complex tachycardia (QRS width ≥ 0.12 second) of three or more consecutive beats at a rate faster than 100 per minute. VT arises from either reentry or automaticity in the ventricular myocardium or Purkinje system below the level of the His bundle. One of the common ways in which VT is classified is whether it is sustained or not. Nonsustained VT (NSVT) is that which terminates spontaneously within 30 seconds without causing severe symptoms. Spontaneous sustained VT requires an intervention, such as cardioversion or antiarrhythmic drug (AAD) administration for termination, or produces severe symptoms, such as syncope, prior to termination. VTs lasting longer than 30 seconds are usually designated as sustained.

Another way to classify VT is based on the QRS morphology (Fig. 41.1). Morphologic classifications include monomorphic VT (the same morphology from beat to beat), polymorphic VT (PMVT, varying morphologies from beat to beat), and sinusoidal VT (when the QRS has a duration similar to that of diastole). Torsades de pointes (TDP) is a unique subcategory of PMVT associated with QT prolongation.

VT can also be classified on the basis of its hemodynamic effects that are largely dependent on the rate of the tachycardia and the presence of underlying myocardial dysfunction. Indeed, for all sustained wide QRS tachycardias the first priority is to determine whether the patient is hemodynamically stable, with adequate blood pressure and perfusion. Pulseless VT is associated with no significant cardiac output and is approached in a similar manner as ventricular fibrillation (VF). VT can also be hemodynamically stable. This hemodynamic classification may be the most relevant classification system for initial management. Continuous electrocardiograph (ECG) monitoring should be implemented and a defibrillator should be at the patient’s bedside for immediate use, even if the patient is hemodynamically stable. If the patient is pulseless and has impaired consciousness, angina, or severe pulmonary edema, prompt electrical cardioversion is warranted. Further therapy after cardioversion is determined by the type of tachycardia and underlying heart disease.

If the patient is hemodynamically stable, a brief history and a 12-lead ECG should be immediately obtained. The immediate history should include determination of known heart disease, in particular prior myocardial infarction, present medications, history of prior arrhythmias, whether the patient has an implanted defibrillator or pacemaker, and drug allergies. A limited initial physical examination should include the cardiovascular system and lungs. A 12-lead ECG should also be obtained following conversion of the tachycardia to compare the tachycardia QRS to that during sinus rhythm, as well as to evaluate underlying events, such as myocardial infarction, and QT interval prolongation, or other changes suggestive of electrolyte abnormalities. Previous ECGs are also helpful in this regard.

Wide QRS Monomorphic Tachycardia

Monomorphic tachycardias have the same QRS configuration from beat to beat (Figs. 41.1A and 41.2). The differential diagnosis of this type of wide QRS complex tachycardia includes VT, supraventricular tachycardia (SVT) with aberrant interventricular conduction (bundle branch block; Fig. 41.3), and pre-excited SVT due to antegrade conduction from atrium to ventricle through an accessory pathway (Fig. 41.4B), or pre-excited QRS complexes during atrial fibrillation (AF) or atrial flutter (Fig. 41.3C). The differentiation is critical for prognosis and long-term management.

Initial Evaluation

Hemodynamic instability is an indication for electrical cardioversion. If the patient is hemodynamically stable, a limited history and physical examination should be performed and a 12-lead ECG obtained. The presence of hemodynamic stability does not indicate that the tachycardia is supraventricular. Hemodynamic stability is dependent on the rate of the tachycardia, underlying ventricular function, and the sympathetic nervous system response to tachycardia. VT can be hemodynamically stable, SVT may cause hemodynamic collapse, and vice versa. Wide QRS tachycardias should be managed as VT unless the diagnosis of SVT can be confirmed. Patients with a history of structural heart disease are more likely to have VT, whereas the absence of structural heart disease favors the diagnosis of SVT. Wide QRS tachycardia in patients with a history of myocardial infarction can be assumed to VT with greater than 95% certainty [1].

The physical examination is occasionally helpful in detecting the presence of dissociation between atrium and ventricle (AV dissociation) confirming VT as the diagnosis. Cannon “a”-waves in the jugular venous pulse occurring intermittently and irregularly during VT indicate periodic contraction of the right atrium against a closed tricuspid valve. AV dissociation may also cause variability in the intensity of the first heart sound and beat-to-beat variability in systolic blood pressure due to the variable contribution of atrial contraction to left ventricular filling. The absence of evidence of AV dissociation does not exclude the diagnosis of VT. Some patients have conduction from ventricle retrogradely over the His-Purkinje system and AV node to the atrium (VA conduction) during VT. Each ventricular beat is accompanied by a cannon “a-wave,” a finding that is also seen in some SVTs (Table 41.1).

Electrocardiogram

VT can be somewhat irregular at its initiation, but persistence of an irregularly irregular wide QRS suggests AF with bundle
branch block or conduction over an accessory pathway rather than VT (Fig. 41.4). Comparing the QRS complex morphology during tachycardia with that of sinus rhythm on an old ECG or following cardioversion can be helpful. An identical QRS morphology during tachycardia and sinus rhythm suggests SVT [2] (with the uncommon exception of bundle branch reentry described later in the chapter). An old ECG may also reveal a short PR interval with δ-waves (Fig. 41.3A) that suggests Wolff–Parkinson–White (WPW) syndrome with an accessory pathway–mediated wide complex tachycardia (WCT; Fig. 41.3B). When the onset of tachycardia is recorded, initiation by a premature P-wave suggests SVT.

Figure 41.1. Three different wide QRS tachycardias are shown. A: monomorphic VT; B: polymorphic VT; and C: sinusoidal VT due to hyperkalemia. VT, ventricular tachycardia.

The following ECG criteria applied in a stepwise approach provide reasonable sensitivity and specificity to differentiate SVT from VT (Figs. 41.5 and 41.6) [3].

Figure 41.2. Sustained monomorphic ventricular tachycardia is present. Dissociated P-waves can be seen (arrows) with occasional fusion beats (stars) that occur when a sinus P-wave occurs with timing appropriate to conduct to the ventricle.

AV dissociation: Dissociation of P-waves (if identifiable) and QRS complexes suggests VT (Fig. 41.2). Because they may be partially buried in the QRS complex, or T-wave, the P-waves may be difficult to identify. Comparison of the contour of QRS and T-waves from beat to beat may be helpful; P-waves may be evident as a slight deflection occurring at regular intervals independent of QRS complexes. AV dissociation is probably the most reliable clue to the diagnosis of VT, especially if a nonsustained run of wide WCT is caught only on a telemetry rhythm strip.

AV dissociation is also indicated by QRS fusion or capture beats. Fusion beats occur when a supraventricular impulse conducts over the AV node and depolarizes a portion of the ventricle simultaneously with excitation from the tachycardia focus. They occur if AV dissociation is present

and the VT is not particularly fast. Fusion beats have a QRS morphology that is typically intermediate between that of a supraventricular beat and a ventricular beat. Capture beats have a similar significance to fusion beats. They occur when a supraventricular beat is able to conduct to the ventricles, depolarizing the ventricle in advance of the next tachycardia beat. These beats are morphologically identical to the QRS complex seen in sinus rhythm but occur in the midst of a wide QRS complex tachycardia.

Figure 41.3. Features of the Wolff–Parkinson–White syndrome leading to pre-excited tachycardias are shown. A: sinus rhythm is shown. The ECG shows a short PR interval and δ-wave. The mechanism is shown in the schematic. Conduction of the sinus impulse (arrows) propagates over the AV node to the ventricles and over the accessory pathway (AP) to the ventricles. Conduction through the accessory pathway is faster than the AV node, producing the δ-wave. B: antidromic AV reentry is present. Tachycardia is due to circulation of the reentry wave front from atrium to ventricle over the accessory pathway, through the ventricle, and retrograde up the AV node to the atrium. Pre-excited antidromic tachycardia is often indistinguishable from ventricular tachycardia. C: atrial fibrillation with rapid conduction over an accessory pathway is shown. Tachycardia is irregular, although at the very rapid rate, the irregularity can be difficult to appreciate.

Figure 41.4. A: A wide QRS tachycardia with a left bundle branch block configuration. B: Following administration of drugs to slow down atrioventricular (AV) conduction atrial flutter is present with a narrow QRS configuration. Thus, A shows atrial flutter with aberrant conduction.

Table 41.1 Supraventricular Tachycardia Versus Ventricular Tachycardia

Findings suggesting ventricular tachycardia
AV dissociation
   Electrocardiogram
      Dissociated P-waves
      Fusion beats, capture beats—indicate conduction of a fortuitously timed P-wave from atrium to ventricle before the ventricle is completely depolarized from the VT focus or circuit
   AV dissociation on physical examination
      Intermittent cannon a-waves in jugular venous pulse
      Beat-to-beat variability in S₁ and systolic blood pressure
ECG leads V₁–V₆
   QRS concordance: The absence of an rS or Rs complex in any precordial lead
   RS > 100 ms: An interval between the onset of the R and the nadir of the S-wave > 100 ms in any precordial lead
Left bundle branch block VT
   Initial R-wave in lead V₁ > 30 ms in duration
   Interval from onset of R to nadir of S in V₁ > 60 ms
   Notching in the downstroke of the S-wave in lead V₁
   In V₆, a QS or QR pattern
Right bundle branch block VT
   V₁: A monophasic R, QR, or RS pattern
   V₆: An R to S < 1 or a QS or a QR pattern

QRS concordance: The absence of an rS or Rs complex in any precordial lead (V₁ to V₆) suggests VT.
RS > 100 ms: An interval between the onset of the R and the nadir of the S-wave greater than 100 ms in any precordial lead (V₁ to V₆) favors VT.

Figure 41.5. The schematic for an algorithm for ECG diagnosis of VT is shown. LBBB, left bundle branch block; RBBB, right bundle branch block; SVT, supraventricular tachycardia, VT, ventricular tachycardia.

Figure 41.6. Electrocardiogram findings indicative of ventricular tachycardia (VT) or supraventricular tachycardia with aberrant conduction are shown. LBB, left bundle branch; RBB, right bundle branch.

If the diagnosis cannot be made after assessment for these features, a more thorough evaluation of the QRS morphology on the 12-lead ECG can be helpful (Fig. 41.6) [3]. For left bundle branch block morphology tachycardias, an initial R-wave in lead V₁ of greater than 30 ms in duration or a duration of greater than 60 ms from the onset of the R-wave to the nadir of the S-wave in V₁ suggests VT. Notching in the downstroke of the S-wave in lead V₁ also suggests VT. In V₆, a QS or QR pattern suggests VT. For right bundle branch block (RBBB) morphology tachycardias, a monophasic R, QR, or RS pattern in V₁ suggests VT. In V₆, an R-to-S amplitude ratio of less than 1 or QS or QR patterns suggests VT.

Electrocardiographic Artifacts that Mimic Wide Complex Tachycardia

Misinterpreting an electrocardiographic artifact, such as the one shown in Figure 41.7, as VT is a common error that has led to inappropriate and invasive procedures including cardiac catheterization, implantation of defibrillators, and even the occasional precordial thump [4]. Normal QRS complexes are often visible marching through the artifact at the sinus rate (arrows in Fig. 41.7). One author has referred to this as the “notches sign” because only small notches may be seen that march through the artifact at intervals that are the same as the RR intervals preceding the onset of tachycardia [5]. The history of the patient’s activity at the time of the recording is often helpful in suggesting artifact. The recording in Figure 41.7 was performed during toothbrushing. Artifacts are also commonly caused by tremors, shivering, and electrical noise. The absence of symptoms or hemodynamic instability during the event (especially if the recording suggested a very fast heart rate) also suggests artifact.

Acute Treatment of Wide Complex Tachycardia

The misdiagnosis of VT as SVT followed by delivery of an inappropriate therapy is common in patients with wide QRS tachycardias [6]. As a general rule, wide QRS tachycardia should be treated as VT unless the diagnosis of SVT can be confirmed.

Figure 41.7. Apparent nonsustained ventricular tachycardia is actually artifact. Arrows indicate the sinus rhythm QRS complexes that “march through” the artifact.

Management of Hemodynamically Unstable VT/VF

Figure 41.8 provides an algorithm for the management of hemodynamically unstable VT or VF. Hemodynamically unstable wide QRS tachycardia that is not due to sinus tachycardia with bundle branch block or artifact requires immediate electrical cardioversion. Both good basic life support (BLS) with prompt and efficient cardiopulmonary resuscitation (CPR) and rapid defibrillation are the most important measures to improve survival in unstable VT/VF [7]. Survival from VT/VF arrest diminishes by 7% to 10% per minute between collapse and defibrillation if CPR is not performed [8]. In fact, several studies have shown that survival from VT/VF arrest can be doubled or tripled if CPR is provided [9,10]. In keeping with these data, the most recent American Heart Association guidelines for cardiopulmonary resuscitation emphasize an integrated strategy of combined CPR and defibrillation [7]. If pulseless VT/VF persists after defibrillation, CPR should be promptly resumed and five cycles completed prior to additional therapy. When VT/VF is revealed during a rhythm check, CPR should be provided while the defibrillator is charging and resumed immediately following shock delivery. The algorithm for VF/pulseless VT should be followed (Fig. 41.8). Either epinephrine or vasopressin can be used as a first-line vasopressor agent if CPR continues to be required after two unsuccessful attempts at cardioversion [7]. If vasopressin is used, a one-time dose is appropriate as it has a half-life of 20 to 30 minutes. Epinephrine can be administered in 1-mg doses every 3 to 5 minutes.

Figure 41.8. The algorithm for management of hemodynamically unstable ventricular tachycardia (VT) or ventricular fibrillation (VF) is shown.

Although definitive evidence of a long-term mortality benefit of any AADs for acute management of VT/VF is lacking, these agents should be used when initial attempts of electrical cardioversion are not successful [11,12]. When VF/pulseless VT persists after three shocks plus CPR and administration of a vasopressor, consider administering an antiarrhythmic, such as amiodarone. If amiodarone is unavailable, lidocaine may be considered. Magnesium should also be considered for TDP associated with a long QT interval [7]. In a trial of 504 patients
with out-of-hospital VF or pulseless VT who failed three attempted cardioversions, administration of 300 mg of intravenous (IV) amiodarone was more effective than placebo for restoration of circulation and survival to hospital admission (44% of treated patients vs. 34% of untreated patients). Survival to hospital discharge was not improved and more patients who received amiodarone had hypotension (59% vs. 48%) or bradycardia (41% vs. 25%) [7,13,14]. Administration of IV procainamide can be considered as an alternative agent, but the data supporting its efficacy are limited [15]. Administration of IV lidocaine is most appropriate in the management of unstable VT/VF during suspected acute myocardial ischemia or infarct [16,17,18].

Although bretylium is an acceptable alternate antiarrhythmic agent for VT, it has been removed from advanced cardiac life support (ACLS) guidelines due to a combination of global supply shortage and lack of evidence showing its superiority over any of the previously mentioned AADs. Bretylium has similar efficacy to amiodarone for treatment of hemodynamically destabilizing VT that has failed cardioversion, but is associated with a greater incidence of hypotension compared to IV administration of amiodarone [7,18].

Management of Hemodynamically Stable Wide QRS Tachycardia

In the absence of signs or symptoms of impaired consciousness or tissue hypoperfusion, a 12-lead ECG should be obtained to attempt to differentiate VT from SVT [7]. In patients in whom the diagnosis of SVT with aberrancy is suspected, the response to vagal maneuvers or adenosine administration while recording the ECG may also elucidate the diagnosis (Fig. 41.4). Vagotonic maneuvers and administration of IV adenosine often terminate or expose SVT and usually have no effect on VT. Close monitoring is required during these maneuvers; hypotension or precipitation of VF can rarely occur.

If the diagnosis remains unknown, the choice of initial antiarrhythmic agent should be influenced by the hemodynamic stability and rhythm analysis (Fig. 41.9). Administration of multiple antiarrhythmic agents should be avoided as polypharmacy increases the risk of precipitating incessant, although usually slower VT or new VTs, such as TDP (see later in the chapter). If the initial agent selected is ineffective, cardioversion is usually warranted.

Figure 41.9. The algorithm for management of hemodynamically tolerated wide QRS tachycardia is shown. AF, atrial fibrillation; SVT, supraventricular tachycardia, VT, ventricular tachycardia.

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