Ventricular Tachycardias

Ventricular tachycardia (VT) is a broad complex tachycardia originating from a ventricular ectopic focus. It is defined as three or more ventricular extrasystoles in succession at a rate of more than 120 beats/minute. Accelerated idioventricular rhythm refers to ventricular rhythms with rates of 100-120 beats/minute.¹

• The rate is usually greater than 120 beats per minute and with broad QRS complexes.
• VT may be monomorphic (typically regular rhythm originating from a single focus with identical or similar QRS complexes) or polymorphic (may be irregular rhythm, with beat to beat variation in QRS complexes).
• Monomorphic ventricular tachycardia is the commonest form of sustained ventricular tachycardia.
• Non-sustained VT is defined as a run of tachycardia of less than 30 seconds duration; a longer duration is described as sustained VT.
• Sustained VT is associated with:
  • Late-phase of myocardial infarction (frequently with left ventricular aneurysm)
  • Cardiomyopathy (including hypertrophic and alcoholic)
  • Right ventricular dysplasia
  • Myocarditis
  • Drugs, e.g. class 1 antiarrhythmics (flecainide, and disopyramide)

Fascicular tachycardia

• Uncommon and not usually associated with underlying structural heart disease.
• It originates from the left bundle branch.
• It produces QRS complexes of relatively short duration (0.11-0.14 seconds) and so is commonly misdiagnosed as a supraventricular tachycardia.
• The QRS complexes have a right bundle branch block pattern.

Right ventricular outflow tract tachycardia

• Originates from the right ventricular outflow tract.
• The ECG typically shows right axis deviation, with a left bundle branch block pattern.
• The tachycardia may be provoked by catecholamine release, sudden changes in heart rate, and exercise.
• It usually responds to drugs such as alpha blockers or calcium antagonists.

Torsades de pointes tachycardia

See separate article on Torsades de pointes.

Polymorphic ventricular tachycardia

• Has the same ECG characteristics as torsades de pointes but in sinus rhythm the QT interval is normal.
• The ECG trace is also similar to that of atrial fibrillation with pre-excitation.
• It is much less common than torsades de pointes.
• If sustained, it often leads to cardiogenic shock.
• It can occur in acute myocardial infarction and may deteriorate into ventricular fibrillation (VF).

• VT is one of the most frequently observed dysrhythmias. VT and coronary disease are common throughout most of the developed world.
• VT incidence rates peak in the middle decades of life, following structural heart disease.

Risk factors

• VT is often a symptom of coronary heart disease or structural heart disease.
• VT can be triggered by electrolyte deficiencies, e.g. hypokalaemia, hypocalcaemia, hypomagnesaemia.
• Use of sympathomimetic agents, e.g. caffeine or cocaine, may stimulate VT in vulnerable hearts.

• Most patients present with symptoms of either ischemic heart disease or haemodynamic compromise resulting from poor perfusion.
• Symptoms may include chest pain, palpitations, dyspnoea, dizziness, syncope and other symptoms of heart failure.
• Signs reflect the degree of haemodynamic instability, including respiratory distress, basal fine lung crepitations, raised JVP, hypotension, anxiety, agitation, lethargy, coma.

• Other tachyarrhythmias, especially other causes of broad complex tachycardia.
  • ECG criteria that support VT over SVT include AV dissociation, fusion beats at the initiation of the arrhythmia, QRS duration over 140 ms, and RS pattern in V1. Patients with underlying structural or ischemic heart disease are more likely to have VT than SVT.
  • ECG criteria that support SVT over VT include a right bundle branch block pattern, varying bundle branch block, an R or qR pattern in V1, or an ectopic P wave preceding the dysrhythmia.
• Heart failure from other causes.
• Myocardial infarction.
• Ventricular fibrillation.

• ECG:²
  • Complexes of atypical morphology often are difficult to interpret. Such tachycardias could be PSVT with aberrant conduction. If patient is unstable, or differentiation between VT and SVT is uncertain, treat rhythm as VT. Some therapies for paroxysmal SVT (e.g. verapamil) can be lethal when employed in VT.
  • No absolute ECG criteria exist for establishing the presence of VT. However, several factors suggest VT, including the following:
    • Rate greater than 100 beats per minute (usually 150-200)
    • Wide QRS complexes (>120 ms)
    • Presence of atrioventricular (AV) dissociation
    • Fusion beats
  • Retrograde ventriculoatrial conduction may occur, which can generate an ECG complex similar to paroxysmal supraventricular tachycardia (PSVT) with aberrant conduction.
• Electrolytes, including serum calcium, magnesium, and phosphate levels. Ionised calcium levels are preferred over total serum calcium. Hypokalaemia, hypomagnesaemia, and hypocalcaemia may predispose patients to either conventional VT or torsade de pointes.
• Levels of therapeutic drugs, e.g. digoxin.
• Evaluate for myocardial ischaemia: serum troponin I levels, or other cardiac markers.
• Chest x-ray: if possibility of congestive heart failure or other cardiopulmonary pathology as contributing factors.

• Arrhythmia may occur with or without either myocardial ischaemia or infarction.
• Accelerated idioventricular rhythm (sometimes termed slow ventricular tachycardia).
• Presents with a rate of 60-100 beats per minute.
• Typically occurs with underlying heart disease (ischaemic or structural).
• It is transient, and only rarely is associated with hemodynamic compromise or collapse.
• Treatment is usually not required unless there is haemodynamic impairment.

Address the ABCs of resuscitation and provide basic life support and advanced life support as necessary, urgent transfer to hospital, venous access, oxygen and ECG rhythm strip monitoring.

Pulseless VT

Is treated as for ventricular fibrillation in line with the advanced life support guidelines from the Resuscitation Council.³

Unstable VT (reduced cardiac output)

• Ventricular fibrillation or pulseless VT is treated by unsynchronised defibrillation; whereas other VT's can be treated with synchronised cardioversion.
• Most patients respond to low levels of energy (e.g. starting at 50 Joules biphasic or 100 Joules monophasic).
• Synchronised defibrillation in unstable VT may cause R-on-T deterioration to VF.
• Defibrillation is followed by airway management if required, supplemental oxygen, vascular access, and antiarrhythmic therapy.
• Advanced cardiac life support: amiodarone is the first line agent for haemodynamically unstable VT.³ Replenishment of magnesium and/or other electrolytes may be a valuable adjunct to antiarrhythmic therapies.⁴

Stable VT

• Stable VT patients do not experience symptoms of haemodynamic decompensation.
• Unlike other dysrhythmias, VT tends to deteriorate into unstable states and more malignant dysrhythmias.
• Therefore stable VT should be treated with lidocaine or timely cardioversion if lidocaine is ineffective.

Refractory VT

• Amiodarone is now preferred over bretylium. Its mechanisms of action are similar, but it is not associated with haemodynamic depression as is bretylium.

Implantable cardioverter defibrillators

NICE Guidance recommends that implantable cardioverter defibrillators should be considered for patients in the following categories:⁵

• Sustained VT causing syncope
• Sustained VT with ejection fraction less than 35%
• Previous cardiac arrest due to VT or VF
• MI complicated by non-sustained VT, or inducible VT on electrophysiological testing, or an ejection fraction less than 35%

• Congestive cardiac failure and cardiogenic shock.
• VT may deteriorate into ventricular fibrillation.⁴

• If treated rapidly, VT generally has a favourable short-term outcome.
• Long-term prognosis depends upon the underlying cardiac disease.