Cardiovascular · PANCE / PANRE

Ventricular Tachycardia and Ventricular Fibrillation

Wide-complex arrhythmia from the ventricle — VF and pulseless VT are cardiac arrest rhythms requiring immediate defibrillation.

Also known as: VT, VF, ventricular tachycardia, ventricular fibrillation, VTach, VFib, wide complex tachycardia

Overview

Ventricular tachycardia is ≥3 consecutive ventricular beats at rate >100 bpm; sustained if >30 s or causes hemodynamic compromise. Ventricular fibrillation is disorganized rapid ventricular electrical activity producing no effective cardiac output.

Epidemiology

Ventricular arrhythmia accounts for the majority of sudden cardiac deaths (~300,000/year US). Most cases occur in patients with structural heart disease, particularly post-MI ischemic cardiomyopathy.

Try two board-style Ventricular Tachycardia and Ventricular Fibrillation questions

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Question 1CardiovascularMedium
A 62-year-old man with dilated cardiomyopathy and an ejection fraction of 25 percent presents after receiving three appropriate implantable cardioverter-defibrillator (ICD) shocks over the past 12 hours, each for sustained monomorphic ventricular tachycardia. He is hemodynamically stable between episodes. Potassium is 4.2 mEq/L and magnesium is 2.1 mg/dL, troponin is not elevated, and device interrogation confirms appropriate detections with no lead malfunction. His beta-blocker has been uptitrated. Which of the following is the most appropriate next step in management?
  • AIntravenous amiodarone with catheter ablation referral
  • BIntravenous procainamide with cardioversion
  • COral sotalol with outpatient follow-up
  • DReprogramming the ICD to a higher detection rate
Reveal answer & full explanation
Correct answer: A — Intravenous amiodarone with catheter ablation referral
  • AIntravenous amiodarone with catheter ablation referral
  • BIntravenous procainamide with cardioversion
  • COral sotalol with outpatient follow-up
  • DReprogramming the ICD to a higher detection rate

Why intravenous amiodarone with catheter ablation referral is correct

  • This patient has ventricular tachycardia (VT) storm, defined as three or more separate episodes of sustained VT or appropriate ICD shocks within 24 hours, here in the setting of dilated cardiomyopathy with severely reduced ejection fraction.
  • Management combines acute antiarrhythmic suppression with definitive substrate-directed therapy: intravenous amiodarone (with continued beta-blockade) acutely suppresses the arrhythmia, and catheter ablation targets the reentrant scar circuit.
  • Amiodarone is the preferred acute antiarrhythmic in structural heart disease; ablation reduces recurrent VT and ICD shocks, as demonstrated in the VANISH and SMASH-VT trials.
  • Reversible triggers such as electrolyte derangement and ischemia have already been excluded here.

Why the others are wrong

  • B) Intravenous procainamide with cardioversion — Although procainamide can terminate stable VT, this patient is hemodynamically stable between episodes and already protected by an ICD, so the priority is suppression plus ablation rather than repeated cardioversion; procainamide is also a negative inotrope poorly tolerated in an ejection fraction of 25 percent.
  • C) Oral sotalol with outpatient follow-up — Sotalol is inadequate for active VT storm, would delay definitive therapy, and carries proarrhythmic and negative inotropic risk in severely reduced systolic function.
  • D) Reprogramming the ICD to a higher detection rate — While antitachycardia pacing and detection programming can reduce unnecessary shocks, programming changes alone do not treat the underlying arrhythmogenic substrate and would leave the patient at continued risk during storm.
Question 2CardiovascularEasy
A 65-year-old male with prior anterior myocardial infarction (MI) presents with palpitations and lightheadedness. ECG shows a regular wide-complex tachycardia at 180 bpm with atrioventricular (AV) dissociation, fusion beats, and QRS duration of 160 ms. Which of the following is the most likely diagnosis?
  • ASupraventricular tachycardia
  • BAntidromic atrioventricular reentrant tachycardia (AVRT)
  • CAtrial flutter with rapid ventricular response (RVR)
  • DVentricular tachycardia
Reveal answer & full explanation
Correct answer: D — Ventricular tachycardia
  • ASupraventricular tachycardia
  • BAntidromic atrioventricular reentrant tachycardia (AVRT)
  • CAtrial flutter with rapid ventricular response (RVR)
  • DVentricular tachycardia

Why Ventricular tachycardia is correct

  • AV dissociation, fusion/capture beats, and QRS >140 ms in a patient with prior structural heart disease are essentially diagnostic of ventricular tachycardia (VT) by Brugada criteria.
  • Prior anterior MI provides the scar substrate for monomorphic re-entrant VT, the most common mechanism in this setting.
  • Default to VT in any patient with prior myocardial infarction (MI) or known coronary artery disease (CAD) presenting with a wide-complex tachycardia until proven otherwise.
  • The regular rate of 180 bpm with a QRS of 160 ms fits a sustained monomorphic VT.

Why the others are wrong

  • Supraventricular tachycardia — a supraventricular rhythm cannot produce AV dissociation or fusion beats; invoking it here is the classic anchoring trap that misclassifies wide-complex VT as "SVT with aberrancy."
  • Antidromic atrioventricular reentrant tachycardia (AVRT) — antidromic AVRT is a supraventricular mechanism; the combination of AV dissociation, structural heart disease, and Brugada criteria makes this a wrong-mechanism confusion with VT.
  • Atrial flutter with rapid ventricular response (RVR) — atrial flutter does not produce AV dissociation or fusion beats, so this is a right-concept-wrong-setting distractor.

Additional high-yield points

  • Stable VT: treat with amiodarone or procainamide.
  • Unstable VT: synchronized cardioversion.
  • AV nodal blockers (verapamil) can be lethal if the wide-complex tachycardia is actually VT.
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Risk factors

  • Coronary artery disease and prior MI (scar-related reentry — most common substrate)
  • Heart failure with reduced EF (LVEF ≤35%)
  • Hypertrophic, dilated, or arrhythmogenic RV cardiomyopathy
  • Inherited channelopathies: long QT, Brugada, catecholaminergic polymorphic VT, short QT
  • Electrolyte abnormalities: hypokalemia, hypomagnesemia, hypocalcemia
  • QT-prolonging drugs: methadone, ondansetron, fluoroquinolones, macrolides, antipsychotics, antiarrhythmics
  • Acute ischemia, myocarditis, cardiac sarcoidosis
  • Stimulant use (cocaine, methamphetamine)

Pathophysiology

Most sustained VT in adults is scar-related macroreentry around fibrotic post-infarct tissue. Triggered activity (early or delayed afterdepolarizations) and abnormal automaticity also produce VT, especially in long QT syndromes (torsades de pointes) and in catecholamine-driven states. VF is multiple wandering wavefronts producing chaotic activation and no coordinated contraction.

Clinical presentation

Symptoms

  • Palpitations, lightheadedness, syncope
  • Chest pain, dyspnea
  • Cardiac arrest in VF or pulseless VT
  • Some patients tolerate sustained monomorphic VT for minutes-hours with mild symptoms

Signs / physical exam

  • Hemodynamic compromise: hypotension, altered mental status, pulmonary edema
  • Cannon A waves (AV dissociation in VT)
  • Variable S1 intensity (AV dissociation)
  • Absent pulse and unresponsiveness in VF / pulseless VT

Differential diagnosis

  • Supraventricular tachycardia with aberrancy — Wide QRS from rate-related or pre-existing bundle branch block; Brugada and Vereckei algorithms favor SVT; respond to adenosine
  • Antidromic AVRT (WPW) — Wide-complex tachycardia in pre-excited patient; treat with procainamide; AVOID AV nodal blockers
  • Pre-excited atrial fibrillation — Irregularly irregular wide complex tachycardia in WPW; can degenerate to VF; treat with procainamide or DC cardioversion
  • Hyperkalemia — Sine wave on ECG, peaked T waves, history of CKD, treat with calcium gluconate, insulin/D50, kayexalate
  • Pacemaker-mediated tachycardia — Paced device patient with rapid wide complex; magnet application terminates
  • Artifact — Patient awake and well-appearing, baseline ECG between artifact, regular underlying rhythm visible

Diagnostic workup

Diagnostic criteria

VT criteria favoring ventricular origin: AV dissociation, capture/fusion beats, QRS >140 ms RBBB or >160 ms LBBB morphology, concordance in precordial leads, extreme axis deviation. When in doubt about wide-complex tachycardia, treat as VT.

Labs

  • BMP, magnesium, calcium
  • Troponin (ischemia), TSH
  • Drug screen if stimulant use suspected
  • Digoxin level if applicable

Imaging

  • 12-lead ECG during tachycardia and after conversion (look for old MI, QT, Brugada pattern, epsilon waves)
  • Echocardiogram — structural disease, EF, scar burden
  • Cardiac MRI for scar mapping, sarcoidosis, ARVC
  • Coronary angiography to evaluate ischemic substrate
  • Electrophysiology study for selected patients and ablation planning

Diagnostic algorithm

flowchart TD
  A[Wide-complex tachycardia] --> B{Pulse?}
  B -->|No| C[Pulseless VT / VF<br/>Defibrillate 200 J<br/>CPR + epi + amiodarone]
  B -->|Yes| D{Hemodynamically<br/>stable?}
  D -->|No| E[Synchronized cardioversion<br/>100 J biphasic]
  D -->|Yes| F[12-lead ECG<br/>IV antiarrhythmic:<br/>amiodarone or procainamide]
  F --> G{Conversion?}
  G -->|No| E
  G -->|Yes| H[Identify cause<br/>Echo, electrolytes, ischemia]
  H --> I{Structural disease?<br/>EF ≤35%?}
  I -->|Yes| J[ICD ± ablation]
  I -->|No| K[Channelopathy workup<br/>or idiopathic VT ablation]
Acute and long-term management of ventricular tachyarrhythmia.

Treatment

First-line

  • PULSELESS VT or VF: immediate unsynchronized defibrillation 200 J biphasic, resume CPR, epinephrine 1 mg IV q3-5 min, amiodarone 300 mg IV bolus then 150 mg, treat reversible H's and T's
  • UNSTABLE VT with pulse (hypotension, altered mental status, ischemia, pulmonary edema): synchronized cardioversion 100 J biphasic
  • STABLE VT with pulse: IV antiarrhythmic — amiodarone 150 mg IV over 10 min, procainamide 20-50 mg/min (preferred for monomorphic VT in many guidelines), or lidocaine 1-1.5 mg/kg IV
  • Torsades de pointes: magnesium sulfate 2 g IV, withdraw QT-prolonging drugs, correct K+ and Mg2+, overdrive pacing or isoproterenol
  • Identify and treat reversible cause: ischemia (revascularize), electrolytes, drugs

Second-line / adjunct

  • ICD — secondary prevention for survivors of cardiac arrest, sustained VT with structural disease, or unexplained syncope with inducible VT
  • Primary prevention ICD: LVEF ≤35% on optimal GDMT (≥3 months) with NYHA II-III; LVEF ≤30% post-MI (after 40 days); selected channelopathies and high-risk HCM
  • Catheter ablation — recurrent VT despite ICD, frequent appropriate shocks, idiopathic monomorphic VT (RVOT, fascicular)
  • Chronic antiarrhythmic therapy: amiodarone, sotalol, mexiletine
  • Beta-blocker baseline for nearly all patients with structural heart disease and VT
  • Wearable cardioverter-defibrillator (LifeVest) as bridge to recovery or ICD

Complications

  • Sudden cardiac death
  • Anoxic brain injury after prolonged arrest
  • Recurrent appropriate ICD shocks (electrical storm)
  • Cardiomyopathy from incessant VT (tachycardia-mediated)
  • ICD complications: lead displacement, infection, inappropriate shocks

PANCE pearls

  • When in doubt about a wide-complex tachycardia, treat as VT until proven otherwise.
  • AV dissociation, capture beats, and fusion beats are highly specific for VT.
  • Torsades de pointes = polymorphic VT with twisting QRS axis in setting of long QT — give magnesium first.
  • Brugada syndrome: pseudo-RBBB with coved ST elevation in V1-V2, autosomal dominant, risk of SCD especially at night; ICD if symptomatic.
  • WPW with atrial fibrillation: AVOID AV nodal blockers (adenosine, beta-blocker, CCB, digoxin) — they accelerate the accessory pathway and can precipitate VF.

Images

Monomorphic ventricular tachycardia — wide-complex tachycardia with uniform QRS morphology
Monomorphic ventricular tachycardia — wide-complex tachycardia with uniform QRS morphology
Ventricular fibrillation — chaotic, disorganized electrical activity; immediate defibrillation indicated
Ventricular fibrillation — chaotic, disorganized electrical activity; immediate defibrillation indicated
Torsades de pointes — polymorphic VT with QRS axis twisting around baseline; associated with prolonged QT
Torsades de pointes — polymorphic VT with QRS axis twisting around baseline; associated with prolonged QT

References

  • AHA 2020 ACLS — 2020 AHA Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care (Panchal et al., Circulation 2020)
  • AHA/ACC/HRS 2017 VA/SCD — 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death (Al-Khatib et al., Circulation 2018)
  • MADIT-II — Prophylactic Implantation of a Defibrillator in Patients with MI and Reduced EF (Moss et al., NEJM 2002)
  • SCD-HeFT — Amiodarone or an ICD for Congestive Heart Failure (Bardy et al., NEJM 2005)

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