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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- VT = broad-complex tachycardia (QRS ≥120 ms, rate 100–250 bpm) arising from the ventricles. Monomorphic (uniform QRS) or polymorphic (varying QRS — includes Torsades de Pointes)
- VF = disorganised, chaotic ventricular depolarisation with no effective cardiac output → cardiac arrest
- Pulseless VT and VF → immediate defibrillation (ALS shockable rhythm algorithm)
- VT with a pulse: if stable → IV amiodarone 300 mg over 20–60 min; if unstable → synchronised DC cardioversion
- Secondary prevention: ICD implantation to prevent sudden cardiac death from recurrent VT/VF
Overview
Ventricular tachycardia (VT) is a broad-complex tachycardia arising from the ventricular myocardium or Purkinje fibres. Sustained VT (lasting >30 seconds or causing haemodynamic compromise) is a medical emergency. VT most commonly occurs in the context of structural heart disease (ischaemic cardiomyopathy, dilated cardiomyopathy, HCM) but can also arise from channelopathies (Long QT syndrome, Brugada syndrome). Ventricular fibrillation (VF) is a chaotic electrical rhythm with no organised contraction and no cardiac output — it is rapidly fatal without immediate defibrillation. VF is the most common rhythm in sudden cardiac death and the most treatable cardiac arrest rhythm.
Epidemiology
VT and VF account for the majority of sudden cardiac deaths. In the UK, sudden cardiac death causes approximately 100,000 deaths per year. The most common underlying cause is ischaemic heart disease (80%). Other causes include cardiomyopathies (DCM, HCM, ARVC), channelopathies (Long QT, Brugada), electrolyte abnormalities (hypokalaemia, hypomagnesaemia), and drug toxicity (digoxin, tricyclic antidepressants, QT-prolonging drugs). In young athletes, HCM and ARVC are the leading causes.
Clinical Features
Symptoms
Palpitations (rapid, regular, broad)
Dizziness, presyncope, or syncope
Chest pain
Dyspnoea
Sudden collapse with loss of consciousness (pulseless VT or VF)
Cardiac arrest — no pulse, no breathing
Signs
Regular broad-complex tachycardia on monitor/ECG (VT)
Chaotic irregular fibrillatory pattern on monitor (VF)
Hypotension, signs of poor perfusion
Cannon A waves in JVP (AV dissociation in VT)
Varying S1 intensity (AV dissociation)
Absent pulse (pulseless VT, VF)
Investigations
First-line
12-lead ECGVT: broad QRS (≥120 ms), regular, AV dissociation, capture/fusion beats confirm VT over SVT with aberrancy. VF: chaotic, irregular, no identifiable QRS
Cardiac monitoringContinuous telemetry — essential for detecting arrhythmia recurrence
BloodsU&Es (K⁺, Mg²⁺), troponin, ABG, drug levels (digoxin)
Second-line
EchocardiographyAssess structural heart disease (LV function, wall motion, HCM, DCM, ARVC)
Coronary angiographyExclude ischaemic substrate if ACS suspected as trigger
Specialist
Cardiac MRITissue characterisation — myocardial scar (DCM), fatty infiltration (ARVC), HCM
Electrophysiology studyMap VT circuit, assess inducibility, guide ablation
Genetic testingIf channelopathy or inherited cardiomyopathy suspected (cascade screening of family)
1
Pulseless VT / VF (cardiac arrest)
- Follow ALS shockable rhythm algorithm — defibrillate immediately
- Adrenaline 1 mg IV after 3rd shock, then every 3–5 min
- Amiodarone 300 mg IV after 3rd shock, 150 mg after 5th shock
- Seek and treat reversible causes (4Hs and 4Ts)
2
VT with pulse — haemodynamically stable
- IV amiodarone 300 mg over 20–60 min (via central line ideally)
- Correct electrolytes: K⁺ to 4.5–5.0, Mg²⁺ to >1.0 mmol/L
- If ischaemia is the trigger → treat ACS
3
VT with pulse — haemodynamically unstable
- Synchronised DC cardioversion under sedation (start at 120–150 J biphasic)
- If refractory → amiodarone IV and repeat cardioversion
4
Torsades de Pointes (polymorphic VT with prolonged QT)
- IV magnesium sulphate 2 g over 10 min (first-line)
- Overdrive pacing (increase heart rate to shorten QT)
- Isoprenaline infusion (if pacing not available)
- Identify and stop causative drugs. Correct electrolytes
5
Long-term prevention
- ICD implantation — recommended for survivors of VT/VF cardiac arrest (secondary prevention) and high-risk patients (primary prevention: LVEF ≤35% despite optimal therapy)
- Catheter ablation — for recurrent VT (reduce ICD shocks)
- Optimise heart failure therapy and manage underlying structural disease
Complications
- Sudden cardiac death: VF is rapidly fatal without defibrillation
- Cardiogenic shock: Sustained VT with very fast rate
- Degeneration: VT → VF → cardiac arrest
- Recurrence: Without ICD or ablation, VT/VF frequently recurs
- ICD-related: Inappropriate shocks, lead complications, infection, psychological impact
UKMLA Exam Tips
- 1If in doubt, treat a broad-complex tachycardia as VT (much more dangerous if misdiagnosed as SVT)
- 2AV dissociation, capture beats, and fusion beats on ECG confirm VT over SVT with aberrancy
- 3Torsades de Pointes = polymorphic VT + long QT → give IV magnesium (NOT amiodarone — amiodarone prolongs QT further)
- 4Amiodarone is the drug of choice for stable monomorphic VT and in the ALS shockable rhythm algorithm
- 5ICD is indicated for secondary prevention (survived VT/VF arrest) and primary prevention (LVEF ≤35%)
- 6Brugada criteria can help differentiate VT from SVT with aberrancy on ECG
practicetest your knowledge on ventricular tachycardia and fibrillationApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — cardiovascular and beyond.
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