Ventricular tachycardia (VT) is an important cause of sudden cardiac death that is estimated to affect between 230,000 and 350,000 people in the United States annually.¹ VT is defined as greater than or equal to 3 beats originating from the ventricles at a rate greater than 100 beats per minute. Sustained VT is defined as lasting longer than 30 seconds or VT requiring intervention for termination because of hemodynamic compromise. Nonsustained VT is defined as lasting less than 30 seconds and self-terminating. VT can be either monomorphic (having the same beat-to-beat electrocardiographic [ECG] morphology) or polymorphic (changing QRS morphology beat to beat). Ventricular fibrillation is defined as rapid and disorganized, irregular electrical activity, typically at a rate greater than 300 bpm (Figure 57.1).

Monomorphic VT and polymorphic VT typically have different underlying mechanisms/pathophysiology. Polymorphic VT may often be driven by ischemia, whereas monomorphic VT is rarely due to an ischemic insult. A form of polymorphic VT, known as torsades de pointes, can be precipitated by a long QT interval. There are many causes of a long QT interval including electrolyte abnormalities, drug effects, or inherited channelopathies. Monomorphic VT is most commonly due to either focal mechanisms (either triggered activity or automaticity) or scar-based reentry (most often in the setting of structural heart disease).² Focal mechanisms are often implicated in idiopathic VT entities, such as outflow tract VTs or Purkinje fiber-associated VTs, which can occur in the absence of structural heart disease; however, their occurrence does not exclude structural heart disease. In contrast to focal VT, the presence of scar promotes a macro-reentrant mechanism for myocardial VT. The heterogeneous conduction properties of scarred myocardium create the critical isthmuses that promote wave break and create excitable gaps, which can sustain a macro-reentrant circuit for monomorphic VT³ (Figure 57.2).

Patients can present with a variety of symptoms depending on the VT characteristics, comorbidities, and underlying etiology. Symptoms can include chest pain, shortness of breath,
palpitations, dizziness, diaphoresis, weakness, and/or syncope. Symptoms are typically abrupt in onset, and if the VT rate is fast, then hemodynamic compromise can be sudden.⁴ Less commonly, if the VT rate is much slower, symptoms can be more subacute if the VT has been ongoing for some time.

As previously mentioned, management of VT initially should follow the algorithm provided by advanced cardiac life support recommendations, with an emphasis on circulatory support and airway protection. Electrical cardioversion is often recommended if VT does not self-terminate. If VT remains refractory to supportive measures, medications should be administered, typically via intravenous formulation. Guideline recommendations suggest the use of amiodarone, sotalol, or procainamide.¹ In the guidelines, procainamide received a stronger recommendation than did amiodarone or sotalol¹; however, this is based on limited data,⁷ and procainamide use is associated with toxicities that require close monitoring. For this reason, in our practice, we prefer the use of amiodarone as an initial agent in cases of refractory VT in the acute setting. Lidocaine has fallen out of favor as a primary agent for management of VT; however, it may still have a role where ischemia is suspected, or when used in combination with other antiarrhythmic agents such as amiodarone.⁸ Lidocaine can also be useful in suppressing arrhythmias in the short term, owing to its short half-life, when subsequent electrophysiology procedures are planned, whereas other agents with longer half-lives could affect arrhythmia inducibility and thus decrease procedural efficacy.

Once stabilized, an evaluation for underlying causes of VT should be performed, such as electrolyte imbalances, drug toxicities, endocrine disorders, inherited channelopathies, or acute coronary syndromes (Algorithm 57.3). If patients continue to have ongoing ventricular arrhythmias in spite of addressing any underlying causes and initiation of antiarrhythmic medications, consideration for intubation and sedation should be made. Advanced imaging such as a cardiac magnetic resonance imaging (MRI) can be performed to assess for myocardial scar, and a positron emission tomography-computed tomography (PET-CT) scan may also be useful in identifying inflammatory conditions such as myocarditis that could be contributing to the arrhythmias.⁹

The management of VT also varies greatly depending on whether it is an idiopathic versus a scar-mediated mechanism. The surface ECG morphology of VT is critical in guiding management because certain 12-lead ECG features can suggest an idiopathic etiology.¹⁰ In cases of scar-mediated VT, the 12-lead ECG can also localize exit sites and direct future invasive procedural management.¹¹