Cardiac Arrhythmias
Ventricular Tachycardia
Wide-QRS rhythm at > 100 bpm — and the dominant mechanism of sudden cardiac death
Ventricular tachycardia is a rapid wide-QRS rhythm from a ventricular focus. Sustained VT lasts > 30 sec and often degenerates into VF. ICDs prevent over 50% of arrhythmic deaths in high-risk patients.
- Definition≥3 beats > 100 bpm; QRS > 120 ms
- Sustained VT≥ 30 sec or hemodynamic collapse
- Monomorphic substrateScar re-entry after MI
- Share of SCD~30% of sudden cardiac death
- Acute treatmentCardioversion 100 J / defib 200 J
- ICD benefit> 50% reduction in arrhythmic mortality
Interactive visualization
Press play, or step through manually. Watch a ventricular focus take over the heart — then degenerate to VF.
Watch the 60-second explainer
A condensed visual walkthrough — narrated, captioned, under a minute.
VT in one paragraph
The ventricles normally activate in 80-100 ms because the impulse rides the high-speed His-Purkinje highway from the AV node down to both bundle branches and out to Purkinje fibers. A rhythm that originates inside ventricular muscle instead — at a scar, a focus, or a triggered cell — must propagate slowly cell-to-cell. Slow propagation produces a wide QRS (> 120 ms). Three or more such beats in a row at > 100 bpm is ventricular tachycardia.
Mechanism — scar re-entry, focal, or triggered
Most monomorphic VT in adults is re-entrant around the border zone of a healed myocardial infarction. The scar contains slow-conducting myocyte channels with surviving cells embedded in fibrotic tissue. When a premature beat finds unidirectional block in one corridor, conduction succeeds through another, and by the time the wave returns it finds the original tissue ready — a stable circuit. The ECG shows a uniform wide QRS because each beat exits the same isthmus.
Polymorphic VT, by contrast, shows beat-to-beat changes in QRS axis. The most important polymorphic VT is Torsades de Pointes — triggered by early afterdepolarizations in long-QT substrates. Other focal VTs include outflow tract VT (idiopathic, often catecholamine-sensitive, ablation-curable) and fascicular VT (verapamil-sensitive).
Worked clinical example
A 67-year-old man with a remote anterior MI presents with palpitations and lightheadedness. Vital signs: HR 178, BP 96/58, alert. ECG: regular wide-complex tachycardia, QRS 160 ms, monomorphic, AV dissociation with occasional fusion beats. Diagnosis: sustained monomorphic VT, presumed scar re-entry around the prior anterior MI territory.
- Initial: O₂, IV access, pads on. He is borderline stable, so begin amiodarone 150 mg IV over 10 minutes; have synchronized cardioversion ready at 100 J biphasic.
- If decompensates: Hypotension → cardiovert at 100 J synchronized. If pulseless → defibrillate 200 J unsynchronized, ACLS protocol.
- Workup: Electrolytes (K 4.0+, Mg 2.0+), troponin, echo (LVEF), ischemic evaluation. Coronary angiography because new VT may herald acute ischemia.
- Long-term: ICD for secondary prevention — sustained VT without a fully reversible cause meets indication. Consider catheter ablation if recurrent shocks or as alternative to chronic antiarrhythmic.
This case is canonical: prior MI provides the substrate, and an ICD will prevent the death that the next episode could otherwise cause. ICD reduces arrhythmic mortality by over 50% in this exact population.
VT vs SVT with aberrancy — the lookup table
| Feature | VT | SVT with aberrancy |
|---|---|---|
| QRS width | Often > 140 ms | Usually 120-140 ms |
| AV dissociation | Yes (P at own rate) | No (1:1 P:QRS) |
| Fusion / capture beats | Diagnostic if present | Absent |
| Axis | Extreme (northwest) | Usually normal |
| Prior MI / structural disease | Strongly favors VT | Less specific |
| Response to adenosine | No effect (usually) | Terminates AV-nodal SVT |
| Initial treatment if unsure | Treat as VT | Treating as SVT is dangerous |
Common mistakes
- Giving verapamil or diltiazem to wide-complex tachycardia. If it is VT, blocking the AV node does nothing useful and the negative inotropic effect can collapse the patient.
- Calling slow regular wide-complex tachycardia "AIVR" and ignoring it. Accelerated idioventricular rhythm at 60-110 bpm during MI reperfusion is benign and self-limited; faster wide-complex demands cardioversion preparation.
- Treating Torsades with amiodarone. Amiodarone prolongs QT and worsens the EAD substrate. Magnesium 2 g IV is correct; isoproterenol or overdrive pacing if refractory.
- Missing the trigger. Electrolyte abnormalities (K, Mg), drugs that prolong QT, ischemia, and decompensated heart failure all provoke VT. Fix the trigger or expect recurrence.
- Delaying ICD discussion. Survivors of sustained VT without reversible cause should leave the hospital with a wearable defibrillator or an ICD already implanted.
Frequently asked questions
What defines ventricular tachycardia?
Three or more consecutive ventricular beats at a rate over 100 bpm. QRS complexes are wide (>120 ms) because the impulse propagates through ventricular muscle without using the rapid His-Purkinje system. Non-sustained VT lasts under 30 seconds. Sustained VT lasts 30 seconds or more or causes hemodynamic compromise. VT may be monomorphic (uniform QRS, typically scar-based re-entry) or polymorphic (changing QRS axis, often triggered activity such as Torsades).
Why does VT cause sudden cardiac death?
Rapid VT prevents the ventricles from filling adequately between beats. Stroke volume falls, cardiac output collapses, and the patient loses consciousness within seconds. VT often degenerates into ventricular fibrillation, where coordinated contraction stops entirely — the heart quivers and produces no output. Without defibrillation within minutes, irreversible brain injury and death follow. VT and VF together cause roughly 30% of all sudden cardiac deaths, and SCD remains a leading cause of death in industrialized nations.
How do you tell VT from SVT with aberrancy?
A wide-QRS tachycardia in someone with structural heart disease is VT until proven otherwise. Specific clues for VT include AV dissociation (P waves marching through QRS at their own rate), fusion beats, capture beats, QRS width over 140 ms, and an extreme axis (northwest). Brugada and Vereckei algorithms formalize these criteria. If uncertain, treat as VT — giving an AV-nodal blocker to true VT can collapse the patient.
What is the acute treatment?
Hemodynamically unstable VT — hypotension, chest pain, altered mental status — gets immediate synchronized cardioversion at 100 J biphasic. Pulseless VT or VF is defibrillation (unsynchronized) at 200 J biphasic. Stable monomorphic VT can be treated pharmacologically: amiodarone 150 mg IV bolus then 1 mg/min, procainamide 20-50 mg/min until termination or hypotension, or lidocaine 1-1.5 mg/kg in ischemic substrate. Polymorphic VT with long QT needs magnesium 2 g IV and correction of electrolytes. ACLS protocols guide pulseless arrest.
When is an ICD indicated?
Secondary prevention: any survivor of cardiac arrest or sustained VT without a reversible cause gets an ICD. Primary prevention: ischemic cardiomyopathy with LVEF ≤35% on guideline-directed medical therapy at least 40 days after MI, or non-ischemic cardiomyopathy with LVEF ≤35% on at least 3 months of therapy. Specific channelopathies (long QT, Brugada, CPVT, hypertrophic cardiomyopathy with risk markers) may indicate ICD even with normal EF. ICDs reduce arrhythmic mortality by over 50% in appropriately selected patients.
What about VT ablation?
Catheter ablation targets the critical isthmus of slow conduction within post-infarction scar — the substrate for monomorphic re-entrant VT. Substrate-based ablation maps low-voltage areas during sinus rhythm; activation mapping is performed during VT if tolerated. Success rates: 60-70% for first procedure in ischemic VT, lower in non-ischemic. Ablation reduces ICD shocks substantially and is now first-line for recurrent monomorphic VT in many patients, often combined with an ICD as backup.
Is non-sustained VT dangerous?
Depends on substrate. In a structurally normal heart and asymptomatic, brief NSVT often requires no specific treatment. In ischemic or hypertrophic cardiomyopathy, NSVT marks elevated risk of sustained VT and SCD. NSVT in HCM with other risk markers (family history, syncope, septum > 30 mm, abnormal blood pressure response) raises ICD threshold. Workup includes echocardiogram, ischemic evaluation, electrolytes, and assessment for inherited arrhythmia syndromes if young.