Overview
Ventricular Tachycardia
Topic Overview
Summary
Ventricular tachycardia (VT) is a wide complex tachycardia (QRS over 120ms) arising from the ventricles. It may be sustained (over 30 seconds) or non-sustained. VT is commonly associated with structural heart disease (ischaemic heart disease, cardiomyopathy). It can be haemodynamically stable or cause pulseless cardiac arrest. Treatment of pulseless VT is immediate defibrillation. Stable VT may be treated with amiodarone or DC cardioversion. Long-term management includes ICD implantation and treatment of underlying cause.
Key Facts
- Definition: VT = 3+ consecutive ventricular beats at over 100 bpm
- ECG: Wide QRS (over 120ms), regular or irregular
- Types: Monomorphic (uniform QRS) or polymorphic (varying QRS, includes torsades)
- Pulseless VT: Shockable rhythm — immediate defibrillation
- Stable VT: Amiodarone or synchronized DC cardioversion
Clinical Pearls
"Wide complex tachycardia is VT until proven otherwise" — safer to assume VT
Torsades de pointes = polymorphic VT with QT prolongation — treat with magnesium
AV dissociation, fusion beats, capture beats = proves VT (not SVT with aberrancy)
Why This Matters Clinically
VT can cause sudden cardiac death. Rapid recognition and treatment are life-saving. In stable patients, distinguishing VT from SVT with aberrancy can be challenging but VT is far more common.
Visual Summary
Visual assets to be added:
- Monomorphic VT ECG
- Polymorphic VT and torsades ECG
- VT vs SVT with aberrancy comparison
- VT management algorithm (ALS)
Epidemiology
Incidence
- Common in patients with structural heart disease
- Leading cause of sudden cardiac death
Demographics
- More common in men
- Average age 60-70 (ischaemic heart disease)
- Younger patients with inherited channelopathies
Causes
| Cause | Notes |
|---|---|
| Ischaemic heart disease | Most common cause; scar-related re-entry |
| Dilated cardiomyopathy | |
| Hypertrophic cardiomyopathy | Risk of SCD |
| ARVC | RV arrhythmogenic cardiomyopathy |
| Channelopathies | Long QT, Brugada, CPVT |
| Drug toxicity | Digoxin, antiarrhythmics |
| Electrolyte imbalance | Hypokalaemia, hypomagnesaemia |
Pathophysiology
Mechanisms
- Re-entry — most common; scar tissue from MI creates circuit
- Triggered activity — afterdepolarisations
- Enhanced automaticity — increased firing from ventricular focus
Why VT is Dangerous
- Rate too fast for effective cardiac output
- May degenerate to VF
- Cardiac arrest
Types
| Type | Features |
|---|---|
| Monomorphic VT | Uniform QRS morphology; usually re-entry |
| Polymorphic VT | Varying QRS; often ischaemia or channelopathy |
| Torsades de pointes | Polymorphic VT with QT prolongation; "twisting of points" |
Clinical Presentation
Symptoms
Signs
Haemodynamic Status
| Status | Features |
|---|---|
| Stable | Conscious, BP maintained |
| Unstable | Hypotension, chest pain, heart failure, reduced GCS |
| Pulseless | Cardiac arrest |
Red Flags
| Finding | Significance |
|---|---|
| Pulseless | Immediate defibrillation |
| Hypotension, reduced GCS | Unstable — DC cardioversion |
| QT prolongation + polymorphic VT | Torsades — magnesium |
Palpitations
Common presentation.
Chest pain
Common presentation.
Dyspnoea
Common presentation.
Dizziness, pre-syncope
Common presentation.
Syncope
Common presentation.
Cardiac arrest (pulseless)
Common presentation.
Clinical Examination
Vital Signs
- Heart rate 140-200+ bpm
- Hypotension (if compromised)
- Tachypnoea
Cardiovascular
- Cannon A waves in JVP
- Varying S1 intensity
- Signs of heart failure
Pulse
- May be absent (pulseless VT)
Investigations
ECG — Critical
| Finding | Significance |
|---|---|
| Wide QRS (over 120ms) | Suggests ventricular origin |
| Regular rhythm | Monomorphic VT |
| AV dissociation | Confirms VT |
| Fusion beats | Confirms VT |
| Capture beats | Confirms VT |
| Concordance | All precordial leads same direction |
Brugada Criteria (VT vs SVT with Aberrancy)
- Absence of RS complex in precordial leads
- RS over 100ms in precordial leads
- AV dissociation
- Morphology criteria for VT
Blood Tests
| Test | Purpose |
|---|---|
| Electrolytes (K+, Mg2+, Ca2+) | Correct abnormalities |
| Troponin | Ischaemia |
| Drug levels | If on antiarrhythmics, digoxin |
Imaging
- Echo: Assess LV function, structural heart disease
- Coronary angiography: If ischaemic cause suspected
Classification & Staging
By Duration
| Type | Definition |
|---|---|
| Non-sustained VT (NSVT) | Under 30 seconds, self-terminating |
| Sustained VT | Over 30 seconds or requires intervention |
By Morphology
| Type | Features |
|---|---|
| Monomorphic | Uniform QRS; single focus |
| Polymorphic | Varying QRS; multiple foci or channelopathy |
| Torsades de pointes | Polymorphic with long QT |
Management
Pulseless VT — Cardiac Arrest
| Action | Details |
|---|---|
| Call for help | Resuscitation team |
| Start CPR | 30:2 |
| Defibrillation | 150-200J biphasic; shockable rhythm |
| Adrenaline | 1mg IV after 3rd shock |
| Amiodarone | 300mg IV after 3rd shock |
| Treat reversible causes | 4Hs and 4Ts |
Unstable VT — With Pulse but Adverse Features
| Action | Details |
|---|---|
| Synchronized DC cardioversion | Up to 3 attempts |
| Then amiodarone | 300mg IV over 10-20 min |
| Or further cardioversion |
Stable VT — Haemodynamically Stable
| Option | Notes |
|---|---|
| Amiodarone | 300mg IV over 20-60 min, then 900mg over 24h |
| Or DC cardioversion | If fails or preferred |
Torsades de Pointes
| Action | Details |
|---|---|
| IV magnesium | 2g IV over 10 min |
| Stop QT-prolonging drugs | Essential |
| Correct K+ | Target over 4.5 |
| Overdrive pacing | If refractory |
| Isoprenaline | To increase heart rate |
Long-Term Management
| Strategy | Indication |
|---|---|
| ICD (implantable cardioverter-defibrillator) | Secondary prevention after VT/VF arrest; primary prevention in high-risk |
| Catheter ablation | Recurrent VT despite ICD |
| Antiarrhythmics | Amiodarone, sotalol, mexiletine |
| Treat underlying cause | Revascularisation, heart failure treatment |
Complications
Acute
- Cardiac arrest (VF, asystole)
- Cardiogenic shock
- Death
Long-Term
- Recurrent VT
- Heart failure
- Stroke (if associated AF)
- ICD shocks
Prognosis & Outcomes
Prognosis
- Depends on underlying heart disease
- VT with preserved LV function: Better prognosis
- VT with reduced EF: Higher mortality without ICD
ICD Outcomes
- Significantly reduces sudden cardiac death
- Appropriate shocks in 20-30% over 5 years
Evidence & Guidelines
Key Guidelines
- Resuscitation Council UK ALS Guidelines
- ESC Guidelines on Ventricular Arrhythmias and SCD
Key Evidence
- ICDs reduce mortality in patients with sustained VT and structural heart disease
- Amiodarone is most effective antiarrhythmic for VT
Patient & Family Information
What is Ventricular Tachycardia?
VT is a fast abnormal heart rhythm that starts in the lower chambers of the heart (ventricles). It can be life-threatening.
Symptoms
- Fast heartbeat (palpitations)
- Dizziness or fainting
- Chest pain
- Collapse
Treatment
- Emergency treatment to restore normal rhythm
- Medication to prevent recurrence
- Often an implanted device (ICD) to shock the heart if VT returns
Resources
References
Primary Guidelines
- Resuscitation Council UK. Advanced Life Support Guidelines. 2021.
- Priori SG, et al. 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J. 2015;36(41):2793-2867. PMID: 26320108
Key Reviews
- Al-Khatib SM, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. Circulation. 2018;138(13):e272-e391. PMID: 29084731