Key Facts

Ventricular tachycardia (VT) is a wide-complex tachycardia originating from the ventricular myocardium or Purkinje system. It is a potentially life-threatening arrhythmia that may degenerate into ventricular fibrillation and cardiac arrest.

Epidemiology

• Most commonly occurs in the context of structural heart disease
• IHD with prior MI is the most common substrate
• Non-sustained VT: common in DCM, HCM, and post-MI patients
• Annual incidence of sudden cardiac death in the UK: ~100,000 out-of-hospital cardiac arrests

Aetiology

• Ischaemic heart disease: myocardial scar from prior MI (most common)
• Cardiomyopathies: DCM, HCM, ARVC
• Inherited channelopathies: long QT syndrome, Brugada, CPVT
• Electrolyte abnormalities: hypokalaemia, hypomagnesaemia
• Drug-induced: class Ic antiarrhythmics (proarrhythmic), digoxin toxicity, QT-prolonging drugs
• Idiopathic: RVOT VT, fascicular VT (structurally normal heart; good prognosis)

Pathophysiology

• Re-entry around myocardial scar tissue (most common mechanism in IHD)
• Triggered activity: afterdepolarisations (digoxin toxicity, catecholamine excess)
• Enhanced automaticity: abnormal impulse generation
• Monomorphic VT: single re-entry circuit or focus (regular, uniform QRS)
• Polymorphic VT: multiple foci or changing circuit (e.g., torsades de pointes)

Classification

• Non-sustained VT (NSVT): ≥3 beats but <30 seconds, self-terminating
• Sustained VT: ≥30 seconds or causing haemodynamic compromise
• Monomorphic: uniform QRS morphology (suggests single focus/circuit)
• Polymorphic: varying QRS morphology (consider ischaemia, torsades de pointes)

Symptoms

• Palpitations
• Dizziness, presyncope, or syncope
• Chest pain
• Dyspnoea
• Cardiac arrest (VF degeneration)

Signs

• Wide-complex tachycardia
• Hypotension
• Cannon A waves in JVP (AV dissociation)
• Variable S1 intensity

Red Flags

• Haemodynamic instability (hypotension, reduced consciousness)
• Pulseless VT (treat as cardiac arrest)
• Polymorphic VT (risk of VF degeneration)
• VT storm: ≥3 episodes of sustained VT within 24 hours

Bedside

• 12-lead ECG: broad complex (≥120ms), rate >100 bpm; look for AV dissociation, capture/fusion beats, concordance
• Continuous cardiac monitoring
• Baseline ECG (post-reversion): look for prior MI (Q waves), long QT, Brugada pattern, ARVC epsilon waves

Bloods

• U&Es: K⁺, Mg²⁺ (hypokalaemia/hypomagnesaemia can trigger VT)
• Troponin: acute ischaemia
• Digoxin level: if on digoxin
• TFTs: thyroid dysfunction
• Drug levels: if relevant

Imaging

• Echocardiography: LV function, structural heart disease, wall motion abnormalities
• Cardiac MRI: scar/fibrosis (late gadolinium enhancement), ARVC assessment
• Coronary angiography: if ischaemic substrate suspected

Special Tests

• Electrophysiology study: inducibility, VT mapping, guide ablation
• Signal-averaged ECG: late potentials (arrhythmogenic substrate)
• Genetic testing: if channelopathy or ARVC suspected

Non-pharmacological

• Pulseless VT: follow ALS algorithm — immediate defibrillation (unsynchronised shock, 150-200J biphasic)
• Continuous cardiac monitoring in ICU/CCU
• Correct electrolyte abnormalities: K⁺ >4.0 mmol/L, Mg²⁺ >1.0 mmol/L

Pharmacological

Acute management:

• Haemodynamically unstable (with pulse): synchronised DC cardioversion (120-150J)
• Stable sustained VT: IV amiodarone 300mg over 20-60 minutes (via central line if possible), then 900mg infusion over 24 hours
• Alternative: IV lidocaine 1-1.5mg/kg bolus (if amiodarone contraindicated)
• Pulseless VT: amiodarone 300mg IV bolus during ALS, further 150mg if refractory

VT storm:

• IV amiodarone
• IV beta-blocker (esmolol)
• Deep sedation/general anaesthesia
• Catheter ablation (urgent)
• Stellate ganglion block

Long-term management:

• Treat underlying cause (revascularisation if ischaemic)
• ICD implantation:
  • Secondary prevention: after sustained VT with structural heart disease
  • Primary prevention: EF ≤35% despite ≥3 months OMT
• Beta-blocker: first-line for suppression
• Amiodarone: adjunct to ICD to reduce shocks
• Sotalol: alternative (combined beta-blocker + class III)

Surgical/Interventional

• Catheter ablation: for recurrent VT, VT storm, or to reduce ICD shocks (especially scar-related VT)
• ICD implantation: gold standard for sudden cardiac death prevention
• Cardiac sympathetic denervation: refractory VT storm

Referral Criteria

• All sustained VT: cardiology/electrophysiology urgent review
• Post-cardiac arrest: consider ICD and ablation
• Recurrent VT/ICD shocks: urgent EP referral
• Suspected channelopathy: specialist inherited cardiac conditions centre

• Sustained VT with structural heart disease: high risk of sudden cardiac death without ICD
• ICD reduces mortality by ~30% in high-risk patients (SCD-HeFT, MADIT-II)
• Idiopathic VT (RVOT, fascicular): benign, curable by ablation (>90% success)
• VT storm: mortality ~15-20% despite treatment
• Post-MI NSVT with low EF: significant risk — ICD indicated
• With optimal management (ICD + medical therapy ± ablation): good long-term outcomes achievable

Brugada Criteria for Differentiating VT from SVT

VT vs SVT with Aberrancy: Key Distinguishing Features