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This is a clinician-written, evidence-based summary aligned to the USMLE Step 2 CK Content Outline. It is intended for medical students preparing for USMLE Step 2 CK. Management reflects current ACC/AHA, USPSTF, and APA guidelines. Always cross-reference with UpToDate, institutional protocols, and clinical judgment.
The Bottom Line
- Wide-complex tachycardia (QRS >120 ms): assume VT until proven otherwise (VT is far more common than SVT with aberrancy)
- Pulseless VT or VF: defibrillation immediately (ACLS algorithm). Epinephrine 1 mg q3-5 min. Amiodarone 300 mg then 150 mg for refractory VF/pulseless VT
- Stable monomorphic VT (with pulse): IV amiodarone or IV procainamide. Synchronized cardioversion if drugs fail
- Polymorphic VT + normal QT = treat like VF (defibrillation, amiodarone). Polymorphic VT + prolonged QT = Torsades de Pointes — treat with IV magnesium, overdrive pacing, and isoproterenol. Amiodarone is CONTRAINDICATED in Torsades
- ICD for secondary prevention after VT/VF arrest; primary prevention if LVEF <=35% on GDMT >=3 months
Overview
Ventricular tachycardia (VT) is a regular wide-complex tachycardia (>=3 consecutive ventricular beats at >100 bpm, QRS >120 ms) originating from the ventricular myocardium or Purkinje system. It is classified as sustained (>=30 seconds or causing hemodynamic compromise) or non-sustained (NSVT, <30 seconds). Ventricular fibrillation (VF) is a chaotic, disorganized ventricular rhythm resulting in no effective cardiac output — it is immediately life-threatening and requires defibrillation. The most common underlying cause of both is structural heart disease (ischemic cardiomyopathy, DCM, HCM).
Epidemiology
Sudden cardiac death (SCD) affects ~350,000 Americans annually, with VT/VF responsible for ~75% of cases. The most common cause of VT/VF is ischemic heart disease (prior MI with scar serving as re-entrant substrate). Other causes: non-ischemic DCM, HCM, ARVC, channelopathies (Long QT, Brugada, CPVT), electrolyte abnormalities (hypokalemia, hypomagnesemia), and drug-induced QT prolongation. Survival from out-of-hospital VF arrest depends critically on time to defibrillation (~7-10% decrease per minute without CPR/defib).
Clinical Features
Symptoms
Palpitations, racing heart
Lightheadedness, presyncope, or syncope
Chest pain (ischemia from reduced diastolic filling time)
Sudden collapse/cardiac arrest (pulseless VT or VF)
Dyspnea (from reduced cardiac output)
Signs
Hemodynamically stable VT: tachycardia, may have AV dissociation signs (cannon A waves in JVP, variable S1 intensity)
Hemodynamically unstable: hypotension, altered mental status, diaphoresis
Pulseless VT/VF: no pulse, unresponsive — cardiac arrest
Investigations
First-line
12-lead ECG (or continuous monitor)Wide QRS (>120 ms) + regular rate = VT until proven otherwise. Features favoring VT over SVT with aberrancy: AV dissociation (most reliable), capture/fusion beats, concordance (all precordial leads same QRS direction), very wide QRS (>160 ms), extreme axis deviation, Brugada criteria. If uncertain: treat as VT — it is safer to treat SVT with aberrancy as VT than to miss true VT
STAT labsBMP (K+, Mg2+, Ca2+), troponin (ACS trigger), ABG/VBG, lactate
Assess QTc on baseline ECGProlonged QTc + polymorphic VT = Torsades de Pointes. Common QT-prolonging drugs: antiarrhythmics (sotalol, dofetilide, amiodarone), antibiotics (macrolides, fluoroquinolones), antipsychotics (haloperidol, ziprasidone), methadone
Second-line
EchocardiogramAssess for structural heart disease (prior MI, cardiomyopathy, ARVC — RV dilation/fat infiltration, HCM)
Coronary angiographyIf ischemic trigger suspected (acute MI causing VT/VF)
Cardiac MRIScar mapping (LGE), ARVC features (RV fat/fibrosis), infiltrative disease
Specialist
EP studyInducibility of VT, mapping for ablation, risk stratification
Genetic testingIf channelopathy suspected: Long QT, Brugada, CPVT, ARVC
1
Pulseless VT or VF (ACLS)
- Immediate defibrillation (unsynchronized shock): biphasic 120-200 J, monophasic 360 J
- Resume CPR immediately after shock for 2 minutes, then reassess rhythm
- Epinephrine 1 mg IV q3-5 min (first dose after initial shock if VF/pVT persists)
- After 2nd shock if still VF/pVT: amiodarone 300 mg IV bolus; if recurs after 3rd shock: amiodarone 150 mg
- Lidocaine IV is alternative if amiodarone unavailable
- Identify and treat reversible causes (Hs and Ts): Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo/hyperkalemia, Hypothermia; Tension pneumothorax, Tamponade, Toxins, Thrombosis (coronary/pulmonary)
2
Stable monomorphic VT (with pulse)
- IV amiodarone 150 mg over 10 min, may repeat; then infusion 1 mg/min x 6h then 0.5 mg/min x 18h
- IV procainamide: alternative (20-50 mg/min until arrhythmia terminates, hypotension, QRS widens 50%, or max dose 17 mg/kg). Preferred by many EP physicians
- Synchronized cardioversion if drugs fail or patient becomes unstable
- IV lidocaine: alternative, especially if ischemic etiology
3
Torsades de Pointes (polymorphic VT + long QT)
- IV magnesium sulfate 2 g bolus (even if Mg level normal) — first-line
- If pulseless: defibrillation (treat like VF)
- Overdrive pacing (temporary transvenous at 90-110 bpm) to shorten QT and suppress pauses
- Isoproterenol IV: temporizing to increase HR and shorten QT
- DISCONTINUE all QT-prolonging drugs immediately
- DO NOT give amiodarone, procainamide, or sotalol — they prolong QT and worsen Torsades
- Correct hypokalemia (target K+ 4.5-5.0) and hypomagnesemia
4
Long-term / secondary prevention
- ICD: Class I for survivors of VT/VF arrest (secondary prevention), or LVEF <=35% on GDMT >=3 months (primary prevention)
- Catheter ablation: for recurrent VT despite ICD + antiarrhythmics (scar-based VT ablation)
- Antiarrhythmic drugs: amiodarone, sotalol, or mexiletine as adjunct to ICD to reduce shocks
- Treat underlying cause: revascularization for ischemic VT, GDMT for HFrEF
Complications
- Sudden cardiac death: VF is immediately fatal without defibrillation
- Cardiogenic shock: Sustained VT with hemodynamic compromise
- ICD shocks: Appropriate (VT/VF terminated) or inappropriate (AF/sinus tach misclassified) — impact quality of life
- Anoxic brain injury: If prolonged arrest before ROSC
USMLE Step 2 CK Exam Tips
- 1Wide-complex tachycardia: ALWAYS assume VT unless proven otherwise. AV dissociation, capture beats, fusion beats, concordance all favor VT
- 2Pulseless VT/VF: defibrillate immediately. Do not delay for IV access, intubation, or other interventions
- 3Torsades de Pointes = polymorphic VT + prolonged QT. Treatment: IV magnesium + overdrive pacing. Amiodarone is CONTRAINDICATED (prolongs QT)
- 4Common QT-prolonging drugs to know: sotalol, dofetilide, haloperidol, droperidol, macrolides (azithromycin), fluoroquinolones (levofloxacin), methadone, ondansetron (high dose)
- 5Brugada pattern: coved ST elevation in V1-V3 + RBBB. Risk of VF. Treatment is ICD (no effective drug therapy)
- 6Epinephrine in ACLS: 1 mg IV q3-5 min. Amiodarone after 2nd shock: 300 mg, then 150 mg
- 7If someone presents with syncope and has an LVEF <=35%: the cause is VT until proven otherwise
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