Diagnosis and management of ventricular tachycardia

Key points

• VT is an arrhythmia with a rate >100 beats per minute arising from the ventricular myocardium or specialised conduction tissue below the penetrating atrioventricular bundle.

• VT can present as an irregular broad complex tachycardia and, therefore, an irregular rhythm does not exclude it as a diagnosis.

• Where there is any uncertainty, particularly in emergent situations, a wide-complex tachycardia should be treated as VT until proven otherwise and, ∼80% of the time, the diagnosis will prove to be VT, especially in patients aged >35 years.

• Most VT occurs in patients with underlying heart disease but ∼10% occurs in those with structurally normal hearts, often arising from the outflow tracts.

• Management of patients with VT can involve risk stratification for sudden cardiac death; the use of implantable cardioverter-defibrillators; suppression of VT through the treatment of any underlying myocardial disease; the use of anti-arrhythmic drugs; catheter ablation; and, in refractory cases, emerging approaches, such as cardiac stereotactic body radiation therapy.

Diagnosis

VT forms an important differential diagnosis for any patient presenting with a regular wide complex tachycardia (WCT), which is a regular heart rhythm demonstrating at least three consecutive beats with a ventricular rate >100 bpm and a prolonged QRS duration (>120 ms) on 12-lead electrocardiogram (ECG).⁷ In addition, VT can present as an irregular rhythm, although irregularity does not exclude VT as a diagnosis. A wide QRS complex indicates a delay in propagation of an electrical impulse throughout the ventricular myocardium and could be the result of slowed or absent conduction in any single portion of the CCS, or origin of a ventricular impulse from a location where it does not engage the CCS. In this case, propagation throughout the ventricles occurs at a slower speed, because of conduction via contractile myocardium as opposed to specialised conduction tissue. In addition to VT, the differential diagnosis for a WCT includes any supraventricular tachycardia (SVT) with associated bundle branch block,⁸ SVT that is conducted to the ventricles via an accessory atrioventricular (or related) pathway (or ‘pre-excited’ SVT), pacemaker-mediated tachycardia, SVT conducted with a delay in myocardial propagation (often because of medication, including class 1A, 1C and class III anti-arrhythmic drugs)⁹ or systemic disturbances¹⁰ resulting in abnormal myocardial electrical propagation.¹¹ When possible, comparison between a resting 12-lead ECG and the WCT is helpful, because it enables a comparison between the morphology of a conducted rhythm and the WCT.

It is generally accepted that the default diagnosis of a WCT on ECG should be considered VT until proven otherwise, particularly in urgent situations.¹¹ This consideration is based on the importance of avoiding administration to patients with VT of medication commonly reserved for the treatment of SVT, which can commonly be associated with haemodynamic deterioration when administered during VT.¹²

Diagnosis of ventricular tachycardia

A definitive diagnosis of VT requires the demonstration of ventriculoatrial dissociation (ie ventricular activation that is independent of atrial activity). With extremely rare exceptions,¹³ this can be considered the case when the number of spontaneous ventricular activations exceeds the number of atrial activations. Alternatives features that can be taken as evidence of AV dissociation include the presence of fusion and capture beats, which are characterised on 12-lead ECG as early beats (ie occurring before the next expected beat of WCT would be seen) with a typical conducted QRS morphology (capture) compared with a 12-lead ECG in sinus rhythm or an intermediate morphology between the WCT and a conducted beat (fusion). AV dissociation can also be demonstrated on 12-lead ECG through cardiac electrical implantable devices (CIED) or by invasive electrophysiology study (Fig 1). When this phenomenon is present, an arrhythmia can be considered ventricular in origin, which could be helpful for guiding immediate and subsequent therapy.

• Download figure
• Open in new tab
• Download powerpoint

Fig 1.

Electrocardiographic diagnosis of ventricular tachycardia (VT). (a) 12-lead electrogram (ECG) showing wide complex tachycardia with right bundle branch block configuration. Diagnosis is made from the regular P-waves, which are dissociated with QRS complexes and indicated by red arrows. (b) Electrograms from an implantable cardiac device (ICD; in this case, a biventricular ICD). Top line (blue) shows nearfield electrical signal on atrial channel, middle line (magenta) shows nearfield electrical signal on right ventricular (RV) channel and bottom line (green) shows far field electrical signal between RV lead tip and left infra-clavicular generator, which can be thought of as a single lead ECG and is used as a discriminator channel to differentiate conducted (ie supraventricular tachycardia; SVT) from ventricular rhythms. On the left-hand side of the panel, there are more signals on the RV channel than on the atrial channel, which is seen to be dissociated from the signal on the ventricular channel, a pattern diagnostic of VT. The device delivers a high-energy shock (indicated) following which the VT terminates and there is a single conducted sinus beat (Vs) followed by resumption of biventricular pacing (BiV). The difference in morphology on the discriminator channel between both the spontaneous beat (V_S) and biventricular paced beats (BiV) can be seen. (c) Data from an electrophysiology study of a patient undergoing VT ablation for recurrent shocks in the context of a non-ischaemic cardiomyopathy. The image demonstrates a catheter entering the left ventricle (LV) through the mitral valve. Colours on the LV shell indicate the measured bipolar voltage and are used as an indication of the health (or otherwise) of the tissue, with purple corresponding to a voltage in the normal range, and red representing severely reduced voltage, found in diseased tissue. A 12-lead ECG of the VT being treated is shown on the right side of the panel. This patient was successfully treated for VT with an ablation procedure and remained free from further shocks during follow-up, which, at the time of writing, was 25 months.

Proof of atrioventricular dissociation is sometimes not possible based on available data when a patient is being assessed and, therefore, a judgement about the likely origin of an arrhythmia must be made instead. Such a judgement can be based on the clinical context in which the arrhythmia occurs, the myocardial substrate that an arrhythmia occurs in and electrocardiographic evidence that might be suggestive, even if not diagnostic, of a ventricular origin for the rhythm. It might be easier to prove that an arrhythmia is not ventricular in origin compared with proving that it is. In the absence of contra-indications, vagal manoeuvres or adenosine can be diagnostically helpful in that they can slow AV conduction, proving SVT, and arrhythmias might terminate following the administration of adenosine, which would be suggestive of a supraventricular arrhythmia, whereas slowing of ventriculoatrial conduction could expose VA dissociation, proving VT.⁹

There are ECG features that are suggestive of VT as opposed to SVT, with some mechanism of QRS broadening. Several algorithms have been proposed to systematically distinguish between VT and SVT (Fig 2).⁹ They typically depend on several principles to indicate the likely origin of a WCT, which include:

• Similarity of QRS morphology to a typical pattern of aberrant conduction: if the QRS complex has a ‘typical’ bundle branch or fascicular block appearance, there is a higher likelihood that the arrhythmia is an aberrantly conducted SVT. If the appearance is not consistent with any combination of bundle branch or fascicular blocks, then the diagnosis is most likely that of pre-excited SVT or VT.

• Ventricular activation speed: this can be considered as the speed of initial ventricular propagation, as defined by the steepness of the initial QRS deflection. A rhythm that is conducted via the CCS will usually be associated with rapid early deflection in the QRS complex. By contrast, impulses arising from a ventricular focus remote from the CCS will usually propagate slowly initially, giving rise to a less steep initial portion of the QRS complex. This has been quantified as an RS interval in any precordial lead of >100 ms (Brugada algorithm)¹⁴ or an R-wave in V1 of >30 ms or >60 ms from QRS onset to the nadir of the S-wave in V1 or V2 (Kindwall criterion).¹⁵ In addition, overall QRS duration >140 ms in a RBBB configuration or >160 ms in a LBBB configuration favours VT.¹⁶

• Relative rapidity of the early portion of ventricular activation compared with the late portion of ventricular activation: this is based on the principle that, during aberrantly conducted SVT, the initial ventricular activation would be rapid, with conduction delay occurring later in the ventricles, whereas, in VT, the initial ventricular activation would be slow because of transmission through myocardial tissue, in contrast to specialised CCS tissue.¹⁷

• Ventricular activation axis: when ventricular activation arises from the apex, the ventricular impulse will spread away from this focus, resulting in a QRS axis in the precordial leads between −90 and −180°, or ‘northwest’. This feature on 12-lead ECG is strongly suggestive of VT. Other QRS axis features that favour VT include left-axis deviation in RBBB morphology tachycardias and right axis deviation in LBBB tachycardias.¹⁸ The polarity of the lead aVR can also be helpful in differentiating the aetiology of a tachycardia. During conducted rhythms, the initial ventricular activation is septal and subsequent ventricular activation proceeds away from the lead aVR, resulting in a predominantly negative QRS complex in the lead aVR. Therefore, rhythms with an initial R wave in the lead aVR (indicating activation toward that lead) strongly suggest VT.⁹ Finally, a significant (>40°) change in axis between sinus rhythm and WCT suggests VT.⁹

• Precordial lead concordance: both positive and negative concordance in the precordial leads are suggestive of VT. Concordance describes uniform polarity of the QRS complexes in the leads in question; for example, positive concordance describes QRS complexes that are positive throughout leads V1–V6. Uncommonly, positively concordant QRS complexes can occur in the context of pre-excited SVT because of a ventricular insertion around the mitral annulus. Negatively concordant QRS complexes in the precordial leads are highly suggestive of VT.

• Download figure
• Open in new tab
• Download powerpoint

Fig 2.

Features on ECG that help in the diagnosis of ventricular tachycardia. Atrioventricular (AV) dissociation is diagnostic of VT. Morphological criteria can be applied depending on the overall similarity of the QRS complex in lead V1 to a typical ‘left bundle branch block’ or ‘right bundle branch block’ morphology. Having differentiated between these, further criteria can be applied. As per the image, QRS duration, precordial lead concordance, and QRS axis all suggest VT. Reproduced via a Creative Commons Attribution-NonCommercial License from Kashou et al.¹⁸

Careful examination of the 12-lead ECG during tachycardia is of value for determining the aetiology of the arrhythmia. Of the algorithms that have been published and validated, the most well known is the Brugada algorithm.¹⁴ Although these algorithms can be extremely helpful, all are subject to misclassification, and all can be ambiguous under some circumstances. Most of these have been validated almost exclusively in patients undergoing electrophysiology study with interpretation by cardiac electrophysiologists outside of the acute clinical setting in which the tachycardia presented.¹⁸ This is important because it gives an indication of why, despite the excellent reported sensitivity and specificity of these algorithms, clinicians in the real world continue to face significant diagnostic uncertainty when interpreting ECGs of WCT. Ultimately, it is likely to be most helpful to apply the principles that the algorithms are derived from rather than to learn the algorithms themselves and be prepared to trial several algorithms in the case of difficulty interpreting a particular algorithm.

VT in structurally abnormal hearts

As noted above, most VTs occur in structurally abnormal hearts. The crucial structural abnormality that underlies most VTs is the presence of myocardial fibrosis.¹⁹ A range of pathologies can result in the development of myocardial fibrosis. These have historically been classified as ischaemic or non-ischaemic.²⁰ Although the label of non-ischaemic cardiomyopathy lacks specificity, it continues to be helpful because it indicates likely differences in the patterns of fibrosis that could be encountered in conditions other than previous myocardial infarction. This is of importance when counselling patients about prognosis, when planning for interventions and the likely success of interventions. A detailed discussion of the differences between substrate in ischaemic and non-ischaemic cardiomyopathies is beyond the scope of this article. However, in both conditions, the mechanism underlying most VTs that are treated is re-entry, which is facilitated by the presence of fibrosis. Re-entry describes a self-sustaining pattern of electrical activation, and is the mechanism underlying most SVTs, including atrial flutter, a more complex form of which also underlies atrial fibrillation.²¹ A re-entrant circuit can be established when a wave of electrical activation passes from a large body of myocardium into a slowly conducting and electrically insulated channel, or ‘isthmus’. As it passes through this isthmus, the recently activated large body of myocardium has the chance to recover excitability. When the wave of activation emerges from the isthmus, the large body of tissue is excitable again and, thus, the emerging wave meets excitable tissue, following which this wave can ‘re-enter’ the isthmus, and the process is repeated. As such, an ‘endless loop’ circuit is established that continues until it is interrupted. Myocardial fibrosis promotes the emergence of re-entry through the slowing of conduction as well as the electrical isolation of myocardial cells that can then behave as an electrically insulated isthmus through which re-entry can occur.

In addition to fibrosis, conditions associated with primary electrical abnormalities, in the absence of structural changes, have been associated with ventricular arrhythmias. These conditions comprise channelopathies, including catecholaminergic polymorphic VT (CPVT), and long-QT syndromes, as well as others.²⁰ These are important because, unlike it often is in overt structural heart disease, the mechanism of VT associated with channelopathies is less likely to be re-entry, given that they are not typically associated with fibrosis. Management should be undertaken in specialist centres with experience in these conditions.

VT in structurally normal hearts

Although the presence of structural heart disease confers a higher likelihood of VT when diagnosing an undifferentiated WCT, up to 10% of VTs occur in the absence of an identified structural abnormality of the heart. The most common site of origin of these rhythms is the ventricular outflow tracts. Outflow tract VTs are associated with characteristically tall QRS complexes in the inferior leads.²² A variety of features on 12-lead ECG can help differentiate a right- from left-sided origin. An example of a VT arising from the RVOT is shown in Fig 3. Although often benign, presentation with outflow tract arrhythmias, in the form of premature ventricular contractions (PVCs) or VT, should prompt careful exclusion of the possibility of an arrhythmogenic cardiomyopathy (AC). Outflow tract arrhythmias in structurally normal hearts are often not associated with haemodynamic compromise.²³ In some cases, they might be associated with tachycardia-induced myopathy²⁴ or sudden-cardiac death.²⁴ Outflow tract arrhythmias are frequently amenable to successful catheter ablation, which is a first-line therapy in symptomatic patients²⁵ and, therefore, patients with symptomatic PVCs/VT with an outflow tract appearance should be referred for electrophysiology consultation to discuss the merits of invasive electrophysiology study. Another distinct arrhythmia encountered in structurally normal hearts is that of fascicular VT. This arrhythmia results from re-entry through a circuit including the fascicles and Purkinje cells in the LV.³ These VTs typically have a right bundle branch block morphology and characteristic narrow QRS complexes with an axis dependent on the fascicle involved in the tachycardia. These are usually haemodynamically well-tolerated rhythms that can be treated with catheter ablation as a first line. When identified, patients with these arrhythmias should be referred to an electrophysiologist for consideration of catheter ablation as a curative option.²⁵

• Download figure
• Open in new tab
• Download powerpoint

Fig 3.

An example of ventricular tachycardia (VT) arising from the right ventricular outflow tract (a) Characteristic 12-lead electrogram (ECG) demonstrating RVOT VT. The QRS is ‘inferiorly directed’, that is, it is predominantly positive in leads II, aVF and III. In the precordial leads, the QRS has a left bundle branch block morphology with a precordial transition (ie the first precordial lead in which a predominantly positive QRS is seen) at lead V4. Note is also made of a QRS complex that is predominantly positive in lead I, indicating a leftward direction of activation. (b) Activation map of the tachycardia shown in (a). Here, the 3D surface represents the right ventricle, with the inflow and outflow valves indicated. The site of origin of the tachycardia is indicated by the arrow, which was the site of successful ablation of the VT.

Management

Acute management of VT is focused on assessing and then stabilising haemodynamic compromise resulting from the arrhythmia. The advanced life support algorithms offer a helpful and practical approach to managing WCT, and appropriate parameters for determining haemodynamic compromise.²⁶ As has been noted, in cases of diagnostic uncertainty, arrhythmias should be treated as ventricular in origin and the administration of medication, such as verapamil, avoided. The most commonly administered anti-arrhythmic drug is amiodarone because of its efficacy and relatively safe short-term safety profile. An important aspect of acute management that might be crucial to guide future arrhythmia management is the acquisition (and storage) of documentary 12-lead ECG evidence of the arrhythmia. The absence of these data can present significant challenges for ongoing care, including decision making around the indication for secondary prevention implantable cardioverter-defibrillators (ICDs).

Ongoing management of patients with VT includes an assessment of the ongoing risk of sudden cardiac death (SCD). In general, ventricular arrhythmias that occur outside of the context of significant systemic disturbance or a reversible cause, and which are associated with haemodynamic instability, represent an indication for consideration of secondary prevention ICD.²⁰ Shared decision making is an important aspect of this process and it is important to discuss both quality of life and longevity alongside an individual patient's goals of care when discussing the option of an ICD.

Suppression of recurrent arrhythmia is another challenge that is important for symptomatic reasons. This might be required as a result of recurrent symptoms of palpitations or in the context of recurrent therapies from an ICD, which can have a profound and debilitating impact on patient wellbeing. The options for suppressing arrhythmias include: treatment of the underlying myocardial disease with guideline-directed medical therapy or of structural abnormalities, such as valvular or coronary disease; the use of anti-arrhythmic drugs; invasive catheter ablation procedures; autonomic modulation, including the use of catheter-based continuous sympathetic blockade or surgical sympathectomy; and emerging non-invasive therapies for VT, such as cardiac stereotactic body radiation therapy (cSBRT).