Cardiovascular

Wide-complex tachycardia: VT vs SVT with aberrancy

Clinical Overview and When to Suspect Wide-Complex Tachycardia

— VT accounts for ~80% of wide-complex tachycardias (WCT) in unselected adults

— In patients with known structural heart disease or prior MI, VT prevalence rises to ~95%

— SVT with aberrancy, pre-excited SVT (WPW + AF/AFL), and paced rhythms make up the remainder

— Age >35, prior MI, cardiomyopathy, reduced LVEF, ICD in place

— Hemodynamic instability does NOT distinguish — both VT and SVT can present unstable

— AV dissociation, capture/fusion beats, or extreme axis on ECG

— Young patient, no structural disease, history of "PSVT," prior identical ECG with same bundle branch block (BBB) morphology at sinus rates

— Onset triggered by typical SVT precipitants (caffeine, anxiety, exercise)

— Pre-excited tachycardia (AF with WPW) — irregular, polymorphic, very rapid (>250 bpm), bizarre QRS

— Hyperkalemia "sine wave" — check K+ early

— Sodium-channel blocker toxicity (TCAs, flecainide) — wide QRS at slower rates

— Pacemaker-mediated tachycardia

Definition: Tachycardia with rate >100 bpm and QRS duration ≥120 ms (≥0.12 s, ≥3 small boxes) on the surface ECG

The core ED question: Is this ventricular tachycardia (VT) or supraventricular tachycardia (SVT) with aberrant conduction?

When to suspect VT first:

When SVT with aberrancy becomes plausible:

Don't-miss mimics:

Step 3 management: When in doubt, treat WCT as VT. Misclassifying VT as SVT and giving AV-nodal blockers (verapamil, diltiazem) can precipitate hemodynamic collapse and is a classic board trap.

Board pearl: A regular monomorphic WCT in a 65-year-old with prior MI is VT until proven otherwise — do not delay cardioversion or antiarrhythmic therapy to "rule out" SVT with aberrancy.

Disposition framing: All sustained WCT requires telemetry admission, electrolyte correction, ischemia workup, and electrophysiology (EP) consultation for long-term rhythm strategy.

Presentation Patterns and Key History

— Sudden onset of palpitations, dyspnea, lightheadedness, chest pressure, or syncope

— May present in cardiac arrest (pulseless VT) — ACLS pathway

— Often in patient with ischemic cardiomyopathy, prior MI, dilated/hypertrophic cardiomyopathy, or ARVC

— Younger patient, prior episodes of "racing heart" that self-terminated or responded to vagal maneuvers/adenosine

— History of WPW, known accessory pathway, or AVNRT

— Symptoms typically less severe but overlap exists

— Prior MI, CABG, PCI, heart failure, reduced EF → shifts probability strongly toward VT

— ICD or pacemaker → consider device-related tachycardia, but also implies underlying substrate for VT

— Family history of sudden cardiac death before age 50 → think long QT, Brugada, ARVC, HCM, catecholaminergic polymorphic VT

— Medication review: QT-prolonging drugs (azithromycin, fluoroquinolones, methadone, ondansetron, antipsychotics), digoxin, antiarrhythmics, illicit stimulants

— Electrolyte risk: diuretic use, vomiting/diarrhea, alcoholism (Mg), CKD/dialysis (K)

— Recent illness: myocarditis prodrome (viral URI → new arrhythmia + troponin leak)

— Exertion-triggered → catecholaminergic polymorphic VT (CPVT), LQT1

— Auditory/emotional trigger → LQT2

— Sleep/rest → LQT3, Brugada

— Post-ischemic chest pain → scar-mediated VT

Classic VT presentation:

Classic SVT-with-aberrancy presentation:

High-yield history elements to elicit rapidly:

Triggers worth asking about:

Key distinction: A patient who tells you "this feels exactly like my SVT before — adenosine fixed it" with a documented prior aberrancy ECG is the rare scenario where SVT with aberrancy is genuinely likely. Without that, default to VT.

CCS pearl: On the CCS interface, order a focused cardiac history, prior ECGs, medication reconciliation, and family history of SCD within the first simulated minutes — these change the pretest probability and downstream orders.

Physical Exam Findings and Hemodynamic Assessment

— Airway, breathing, circulation — pulse present or absent?

— Pulseless WCT → defibrillate (unsynchronized) and run pulseless VT/VF algorithm

— Pulse present → assess stability: hypotension (SBP <90), altered mental status, ischemic chest pain, acute heart failure, or shock

— Unstable WCT with a pulse → immediate synchronized cardioversion (100 J biphasic, escalate as needed); if polymorphic/unable to sync → defibrillate

— Stable → time to obtain a 12-lead ECG and consider pharmacologic conversion

— Cannon A waves in the jugular venous pulse — intermittent large pulsations from atrial contraction against closed tricuspid valve

— Variable intensity of S1 — changing PR relationship

— Beat-to-beat variation in systolic blood pressure

— These three findings together are highly specific for AV dissociation → VT

— Displaced/sustained apical impulse → LV dysfunction

— S3 gallop → heart failure

— Prior sternotomy scar → CABG/valve history

— ICD/pacemaker pocket → device-related considerations

— A "stable-looking" patient can decompensate in seconds — keep pads on, IV access ×2, defibrillator at bedside

— Borderline BP (90s systolic) with mentation intact is still "stable" by ACLS but warrants aggressive monitoring

Initial assessment priorities (ACLS framework):

Stable vs unstable:

Exam clues suggesting VT (AV dissociation):

Signs of underlying structural disease:

Hemodynamic pitfalls:

Step 3 management: For any unstable WCT with a pulse, the answer on exam is synchronized cardioversion — not adenosine, not amiodarone bolus first. Sedate if time permits (etomidate or midazolam) but do not delay cardioversion for sedation in extremis.

Board pearl: Cannon A waves + variable S1 + beat-to-beat BP variability = AV dissociation = VT. Memorize this triad — it shows up as a written-stem giveaway when ECG is not provided.

Diagnostic Workup — ECG and Initial Labs

— AV dissociation — independent P waves marching through QRS complexes (pathognomonic when present)

— Capture beats — narrow QRS interrupting WCT (sinus impulse captures ventricle)

— Fusion beats — hybrid QRS morphology (sinus + ventricular)

— QRS duration >140 ms (RBBB morphology) or >160 ms (LBBB morphology)

— Extreme axis (northwest axis, −90° to ±180°): positive in aVR, negative in I and aVF

— Concordance across precordial leads (all V1–V6 same polarity — all positive or all negative)

— Monomorphic regular rhythm at 130–200 bpm

— Typical RBBB or LBBB pattern matching prior sinus ECG

— Onset with a premature P wave

— Response to vagal maneuvers

— 1. Absence of RS complex in all precordial leads → VT

— 2. R-to-S interval >100 ms in any precordial lead → VT

— 3. AV dissociation → VT

— 4. Morphology criteria in V1 and V6 → VT

— BMP (K+, Mg2+, Ca2+, renal function), CBC, troponin, TSH, lactate, ABG/VBG

— Drug levels if relevant (digoxin), urine tox screen

— Beta-hCG in reproductive-age women before imaging/medications

The 12-lead ECG is the central diagnostic tool — obtain immediately, but never delay cardioversion in the unstable patient

Features strongly favoring VT:

Features favoring SVT with aberrancy:

Brugada criteria (simplified, 4 steps):

Vereckei aVR algorithm: Initial R wave in aVR, or initial r/q >40 ms, or notch on downstroke → favors VT

Initial labs to order in parallel:

CCS pearl: Order continuous telemetry, IV access ×2, defibrillator pads on patient, 12-lead ECG, BMP, Mg, troponin, and CXR simultaneously in the ED — these are the first-minute orders graded on a WCT case.

Board pearl: Concordance + AV dissociation + extreme axis = VT, full stop. Don't get distracted by stability.

Advanced and Confirmatory Studies

— If a prior sinus-rhythm ECG shows the identical BBB morphology as the current WCT, SVT with aberrancy becomes much more likely

— Conversely, a different QRS morphology in tachycardia vs baseline favors VT

— Obtain after stabilization in all patients with new sustained WCT

— Assess LVEF, wall motion abnormalities (ischemic scar), chamber dimensions, valvular disease, hypertrophy

— LVEF ≤35% is a key threshold for ICD eligibility for primary prevention

— Serial troponins; if elevated or ischemic ECG features → cardiology consult, consider coronary angiography

— VT in setting of acute ischemia is treated by revascularization plus antiarrhythmic

— Identifies scar (late gadolinium enhancement), infiltrative disease (sarcoidosis, amyloidosis), ARVC, myocarditis

— Increasingly the gold standard for arrhythmogenic substrate characterization

— Definitive for mechanism — inducibility of VT, mapping for ablation, distinguishing scar-mediated VT from idiopathic VT (e.g., RVOT, fascicular)

— Adenosine challenge in stable, regular, monomorphic WCT: terminates SVT (and some idiopathic outflow-tract VTs), no effect on most scar-mediated VT — but only in stable patients and with defibrillator ready

— Consider for suspected channelopathies (LQTS, Brugada, CPVT) or familial cardiomyopathy

— Cascade screening of first-degree relatives if positive

Comparison with prior ECGs:

Echocardiography (TTE):

Ischemia evaluation:

Cardiac MRI:

Electrophysiology study (EPS):

Genetic testing:

Step 3 management: After acute stabilization, the next steps are echo, ischemia workup, and EP referral. ICD evaluation is mandatory for patients who survive hemodynamically significant VT/VF not due to a reversible cause.

Key distinction: Idiopathic VT (RVOT, fascicular) occurs in structurally normal hearts, often responds to verapamil (fascicular) or beta-blockers (RVOT), and has an excellent prognosis — but the diagnosis is made by EP, not in the ED.

Risk Stratification and First-Line Management Logic

— Pulseless → defibrillate at 200 J biphasic, CPR, epinephrine, amiodarone 300 mg IV push, treat reversible causes (Hs and Ts)

— Pulse + unstable (hypotension, altered mental status, ischemic chest pain, acute HF) → synchronized cardioversion 100 J biphasic, escalate

— Pulse + stable → pharmacologic conversion attempt, then cardioversion if fails

— Procainamide 20–50 mg/min IV until arrhythmia suppressed, hypotension, QRS widens >50%, or max 17 mg/kg (PROCAMIO trial favored procainamide over amiodarone for efficacy and safety)

— Amiodarone 150 mg IV over 10 min, may repeat, then 1 mg/min infusion ×6 h then 0.5 mg/min

— Sotalol 100 mg IV over 5 min (less commonly used acutely)

— With long QT (Torsades de pointes) → IV magnesium 2 g, correct K+ to >4.0, withdraw QT-prolonging drugs, overdrive pacing or isoproterenol if recurrent

— With normal QT → likely ischemic; treat as VT, urgent ischemia workup, consider amiodarone and beta-blockade

— Vagal maneuvers (Valsalva, modified Valsalva with leg raise)

— Adenosine 6 mg IV push → 12 mg → 12 mg — only if regular and monomorphic, with defibrillator ready

— Do NOT give adenosine to irregular WCT (could be AF with WPW — risk of VF)

The decision tree starts with stability and pulse:

Stable monomorphic WCT — three reasonable options:

Stable polymorphic WCT:

Suspected SVT with aberrancy in a stable patient:

Reversible causes to address concurrently: electrolytes (K, Mg, Ca), ischemia, hypoxia, acidosis, drug toxicity, hypothermia

Step 3 management: When the rhythm is irregular, wide, and very fast (>200 bpm), think AF with WPW. Treat with procainamide or synchronized cardioversion. Avoid AV nodal blockers (adenosine, beta-blockers, calcium channel blockers, digoxin) — they accelerate conduction down the accessory pathway and can precipitate VF.

Board pearl: "ABCD" drugs to avoid in pre-excited AF: Adenosine, Beta-blockers, Calcium channel blockers, Digoxin.

Pharmacotherapy — First-Line Drug Regimen

— Dose: 20–50 mg/min IV loading until rhythm conversion, hypotension, QRS widens >50%, or 17 mg/kg total; maintenance 1–4 mg/min

— First-line for stable monomorphic VT per PROCAMIO trial (higher conversion, fewer major adverse cardiac events vs amiodarone)

— Also first-line for pre-excited AF (AF with WPW) — slows accessory pathway conduction

— Avoid in: prolonged QT, severe heart failure, myasthenia gravis, severe renal impairment (NAPA accumulation)

— Monitor BP, QRS width, QT continuously during infusion

— Dose: 150 mg IV over 10 min, may repeat once for breakthrough; then 1 mg/min ×6 h, then 0.5 mg/min ×18 h

— Preferred when LV dysfunction or heart failure coexists (negative inotropy minimal)

— Adverse effects acutely: hypotension (rate of infusion), bradycardia, phlebitis (use central line for prolonged infusion)

— Dose: 1–1.5 mg/kg IV bolus, may repeat 0.5–0.75 mg/kg; infusion 1–4 mg/min

— Particularly useful in ischemia-driven VT (acute MI)

— Toxicity: CNS (perioral numbness, tinnitus, seizures), worsens with hepatic dysfunction

— 2 g IV over 1–2 min for Torsades de pointes, even with normal serum Mg

— Repeat dose then infusion 1–2 g/h if recurrent

— Useful adjunct in electrical storm (≥3 episodes VT/VF in 24 h), especially post-MI or sympathetic-driven

— Esmolol 500 mcg/kg bolus, 50–200 mcg/kg/min infusion

Procainamide (Class IA):

Amiodarone (Class III):

Lidocaine (Class IB):

Magnesium sulfate:

Beta-blockers (esmolol, metoprolol):

Adenosine — only for stable, regular, monomorphic WCT when SVT with aberrancy is genuinely suspected; can also unmask atrial flutter

Step 3 management: In a patient with known LV dysfunction (EF <40%) and stable VT, amiodarone is preferred over procainamide due to procainamide's negative inotropy and hypotension risk.

Board pearl: Polymorphic VT + long QT + low Mg/K = give magnesium first, then correct electrolytes, then withdraw offending QT-prolonging drugs.

Procedures — Cardioversion, Defibrillation, and Ablation

— Indication: unstable WCT with a pulse, or stable WCT refractory to drugs

— Energy: biphasic 100 J initial for monomorphic VT, escalate to 150, 200, 360 J as needed

— Sedation: etomidate 0.1–0.2 mg/kg or midazolam 1–2 mg + fentanyl 50–100 mcg if hemodynamics permit; don't delay if extremis

— Pad placement: anterior-lateral or anterior-posterior; remove transdermal patches (nitro)

— Pulseless VT/VF or polymorphic VT (unable to sync on irregular QRS)

— Biphasic 200 J initial, continue per ACLS

— Secondary prevention: survivors of cardiac arrest, sustained VT with structural heart disease, syncope with inducible VT — all qualify

— Primary prevention: LVEF ≤35% with NYHA II–III HF on optimal medical therapy for ≥3 months post-MI or ≥3 months from diagnosis of nonischemic CM; ischemic CM with EF ≤30% and NYHA I

— Wearable defibrillator (LifeVest) as bridge during the 90-day post-MI waiting period

— Indicated for recurrent monomorphic VT despite antiarrhythmics, ICD shocks, idiopathic VT (RVOT, fascicular — often curative), and electrical storm

— Substrate mapping for scar-mediated VT

— Deep sedation, intubation, stellate ganglion blockade, mechanical circulatory support (IABP, Impella, VA-ECMO)

— Urgent EP consultation for ablation

— Useful in pause-dependent Torsades; transvenous or transcutaneous pacing at 90–110 bpm shortens QT and prevents recurrence

Synchronized cardioversion:

Unsynchronized defibrillation:

ICD placement:

Catheter ablation:

Temporary measures for electrical storm:

Overdrive pacing:

Step 3 management: After successful conversion of sustained VT in a patient with structural heart disease, the disposition is ICU/telemetry admission, echo, ischemia workup, and EP consult for ICD evaluation before discharge.

CCS pearl: Don't forget post-cardioversion orders: repeat 12-lead ECG, continuous telemetry, electrolyte repletion to K >4 and Mg >2, and cardiology consult — these are sequence-graded.

Special Populations — Elderly and Renal/Hepatic Impairment

— Higher prevalence of structural heart disease → WCT is VT until proven otherwise

— Polypharmacy increases risk of drug-induced QT prolongation (azithromycin, fluoroquinolones, antipsychotics, SSRIs, ondansetron)

— Reduced clearance of antiarrhythmics — start lower, titrate slower

— Higher risk of digoxin toxicity → bidirectional VT, frequent PVCs, AV block; treat with digoxin-specific Fab fragments

— Procainamide: active metabolite NAPA renally cleared — accumulates in CKD, causing QT prolongation and Torsades; avoid or dose-reduce significantly if CrCl <50

— Sotalol: renally cleared, contraindicated if CrCl <40, requires inpatient initiation with QT monitoring

— Dofetilide: strict renal dosing, contraindicated if CrCl <20, mandatory 3-day inpatient telemetry initiation

— Amiodarone: hepatic metabolism — preferred in renal failure

— Lidocaine: safe in renal failure but hepatic clearance — careful in liver disease

— Lidocaine and amiodarone both hepatically metabolized — reduce dose, monitor for CNS toxicity (lidocaine) and bradycardia/hepatotoxicity (amiodarone)

— Amiodarone causes hepatitis in ~3% — monitor LFTs at baseline, 6 months, annually

— High prevalence of LVH, CAD, electrolyte shifts → sudden cardiac death is leading cause of mortality

— Avoid intradialytic hypokalemia (use K bath ≥2)

— ICD eligibility same as general population but mortality benefit attenuated

— Check and correct K+ to >4.0 and Mg2+ to >2.0 in all WCT patients

— Hyperkalemia → sine-wave WCT mimicking VT; treat with calcium gluconate, insulin/glucose, bicarbonate, dialysis

Elderly patients:

Renal impairment:

Hepatic impairment:

Dialysis patients:

Electrolyte derangements drive arrhythmia in elderly/CKD:

Step 3 management: In an elderly CKD patient with WCT, choose amiodarone over procainamide or sotalol — and confirm potassium and magnesium are repleted before any antiarrhythmic.

Board pearl: Bidirectional VT in an elderly patient on a thiazide and digoxin = digoxin toxicity — give Fab fragments, do not cardiovert unless unstable.

Special Populations — Pregnancy, Pediatrics, and Genetics

— Hemodynamic and hormonal changes increase arrhythmia frequency; most are benign SVT, but new VT warrants workup for peripartum cardiomyopathy

— Synchronized cardioversion is safe in all trimesters — fetal monitoring during procedure, left lateral tilt to avoid IVC compression

— Adenosine is safe in pregnancy (does not cross placenta significantly)

— Beta-blockers: metoprolol or labetalol preferred; avoid atenolol (fetal growth restriction)

— Amiodarone: avoid if possible — fetal hypothyroidism, neurodevelopmental effects; use only if life-threatening arrhythmia refractory to alternatives

— Procainamide is reasonable acutely; lidocaine acceptable

— Postpartum: think peripartum cardiomyopathy → echo, BNP

— WCT in children is rare; SVT with aberrancy more common than in adults

— Congenital heart disease (especially post-tetralogy of Fallot repair), congenital LQTS, CPVT, HCM are key substrates

— Dosing: amiodarone 5 mg/kg IV; cardioversion 0.5–1 J/kg, escalate to 2 J/kg; defibrillation 2 J/kg → 4 J/kg

— Always screen for congenital channelopathy with detailed family history of SCD, drowning, unexplained MVA

— Long QT syndrome (LQTS): congenital (KCNQ1/LQT1 exertional, KCNH2/LQT2 auditory, SCN5A/LQT3 sleep); treat with beta-blockers (nadolol or propranolol), avoid QT-prolonging drugs, ICD if syncope on therapy

— Brugada syndrome: SCN5A, type 1 pattern (coved ST in V1–V2), treat fever aggressively, avoid sodium-channel blockers, quinidine, isoproterenol for storm, ICD if symptomatic

— CPVT: RYR2, exertion/emotion-triggered bidirectional VT, treat with beta-blockers ± flecainide, exercise restriction, ICD selectively

— ARVC: desmosomal genes, RV dilation, epsilon waves, T-wave inversions V1–V3, exercise restriction critical

Pregnancy:

Pediatrics:

Inherited arrhythmia syndromes:

Step 3 management: Any pregnant patient with hemodynamically unstable WCT gets synchronized cardioversion immediately — fetal safety follows maternal stability.

Key distinction: Sudden death in a young athlete on the field → consider HCM, ARVC, CPVT, anomalous coronary, commotio cordis — order family screening and genetic counseling for survivors and relatives.

Complications and Adverse Outcomes

— Cardiac arrest and sudden cardiac death — VT degenerating to VF

— Cardiogenic shock from prolonged tachycardia and loss of AV synchrony

— Tachycardia-mediated cardiomyopathy if untreated for days–weeks (often reversible after rate/rhythm control)

— Acute pulmonary edema in patients with reduced LVEF

— Myocardial ischemia — increased demand, reduced diastolic filling

— Thromboembolism — particularly after cardioversion of unrecognized AF with WPW

— Cardioversion: skin burns, post-shock arrhythmias (bradycardia, asystole), thromboembolism if AF >48 h without anticoagulation, aspiration during sedation

— ICD complications: lead dislodgment, pneumothorax, infection (pocket or endocarditis), inappropriate shocks (10–20% lifetime), psychological distress, PTSD-like syndrome after multiple shocks

— Catheter ablation: cardiac tamponade, AV block, stroke, vascular access complications, esophageal injury (LA ablation), phrenic nerve injury

— Procainamide: hypotension, QT prolongation/Torsades, drug-induced lupus (positive ANA in 50% at 1 year), agranulocytosis

— Amiodarone (long-term): pulmonary fibrosis (1–17%, dose-dependent), thyroid dysfunction (both hyper- and hypo-), hepatitis, corneal microdeposits, blue-gray skin, peripheral neuropathy, optic neuropathy

— Sotalol/dofetilide: Torsades, especially with renal impairment, hypokalemia, hypomagnesemia

Acute complications of VT:

Procedural complications:

Drug-related complications:

Electrical storm: ≥3 episodes of sustained VT/VF or appropriate ICD shocks within 24 hours — high mortality, requires ICU admission, deep sedation, beta-blockade, amiodarone, and emergent EP consult for ablation

Inappropriate ICD shocks: often triggered by AF with rapid ventricular response or SVT misidentified by device — adjust device programming, treat underlying arrhythmia

Step 3 management: Any patient receiving ≥3 ICD shocks in 24 hours needs emergent ED evaluation, telemetry admission, magnet over device (if shocks inappropriate), and EP consult — do not send home.

Board pearl: New cough, dyspnea, and bilateral interstitial infiltrates on a patient on amiodarone = amiodarone pulmonary toxicity — stop drug, start steroids, get high-resolution CT and PFTs.

When to Escalate — ICU, Consult, and Inpatient Triage

— Sustained VT requiring cardioversion or antiarrhythmic infusion

— Electrical storm

— Post-cardiac arrest care (targeted temperature management 32–36°C, hemodynamic support, neuroprognostication delayed ≥72 h)

— Hemodynamic instability or vasopressor requirement

— Active ischemia driving arrhythmia

— Concurrent intubation/sedation needs

— Stable patient post-conversion with structurally normal heart pending workup

— Antiarrhythmic initiation requiring QT monitoring (sotalol, dofetilide — mandatory inpatient telemetry for ≥3 days/5 doses)

— Cardiology/EP: all sustained WCT — for mechanism determination, antiarrhythmic strategy, ICD eligibility, ablation candidacy

— Interventional cardiology: if ischemia is suspected driver

— Cardiothoracic surgery: if mechanical complications (LV aneurysm, post-MI VSD, papillary muscle rupture) drive substrate

— Genetics/inherited arrhythmia clinic: for channelopathies, ARVC, HCM

— Community ED without EP services should transfer hemodynamically stable patients with sustained VT to a tertiary center after acute stabilization

— Pre-transfer: pads on, IV access, antiarrhythmic infusion running, ACLS-capable transport

— Any documented sustained VT

— Syncope with structural heart disease or abnormal ECG

— Family history of SCD in a patient with new arrhythmia

— Electrolyte derangement not yet corrected

— New troponin elevation

— New reduced LVEF on bedside echo

ICU admission indicators:

Step-down/telemetry:

Consultations to initiate from the ED:

Transfer considerations:

Disposition red flags requiring admission (do not discharge):

CCS pearl: For a CCS case of sustained VT, the order sequence is: ACLS → defibrillation/cardioversion → IV antiarrhythmic → electrolyte repletion → ECG → labs → echo → telemetry/ICU admit → cardiology + EP consult → ischemia workup. Skipping ICU admission for a converted VT patient with structural disease loses points.

Step 3 management: All survivors of sustained VT or VF not due to a fully reversible cause need ICD evaluation before discharge — defer discharge until EP has weighed in.

Key Differentials — Same-Category (Wide-Complex) Rhythms

— Regular, uniform QRS morphology

— Scar-mediated (post-MI, ARVC, cardiomyopathy) most common

— Idiopathic VT subtypes: RVOT VT (LBBB + inferior axis, in structurally normal hearts), fascicular VT (RBBB + left axis, verapamil-sensitive)

— QRS morphology varies beat to beat

— Long QT–associated → Torsades de pointes — treat with Mg, correct K, withdraw offending drugs, overdrive pacing

— Normal QT → ischemic — treat ischemia, beta-blockade, amiodarone, urgent angiography

— CPVT (bidirectional VT) — exertion-triggered, beta-blockers

— Brugada-associated — fever, sodium-channel blockers as triggers; treat with isoproterenol, quinidine

— Chaotic, no discernible QRS — pulseless — defibrillate

— Wide-complex, regular, rate 50–120 bpm — too slow to be VT

— Classic for reperfusion after thrombolysis or PCI for STEMI — benign, no treatment

— Sinus tach, atrial tach, AVNRT, AVRT, atrial flutter — all conducted with BBB

— Morphology matches prior sinus BBB pattern; response to vagal/adenosine

— Irregularly irregular (AF) or regular (flutter), very rapid (often >250 bpm), bizarre/changing QRS morphology

— Treat with procainamide or cardioversion; avoid AV nodal blockers

— Regular WCT with conduction down accessory pathway and up AV node

— Looks identical to VT — treat as VT if uncertain

— Pacer spikes preceding each QRS — interrogate device

Within the WCT differential, distinguish:

Monomorphic VT:

Polymorphic VT:

Ventricular fibrillation:

Accelerated idioventricular rhythm (AIVR):

SVT with aberrancy:

Pre-excited tachycardias (AF or atrial flutter with WPW):

Antidromic AVRT:

Paced rhythm:

Key distinction: Regular monomorphic WCT at 130–180 bpm with prior MI = VT; irregular polymorphic WCT >250 bpm with delta-wave-like QRS = pre-excited AF; wide-complex rhythm at 60–110 bpm after PCI = AIVR (leave alone).

Key Differentials — Other-Category Mimics and Confounders

— K+ >6.5: peaked T waves → PR prolongation → QRS widening → sine-wave pattern that mimics VT/VF

— Treat with calcium gluconate immediately, then insulin/D50, albuterol, bicarbonate, kayexalate/patiromer/lokelma, dialysis

— Always check K+ in any new WCT — hyperkalemia is a reversible "VT mimic"

— TCAs (amitriptyline, nortriptyline), flecainide, propafenone, cocaine, diphenhydramine in massive overdose, bupropion

— Wide QRS, terminal R wave in aVR >3 mm, hypotension, seizures, anticholinergic features

— Treat with sodium bicarbonate 1–2 mEq/kg IV bolus, titrate to QRS narrowing and pH 7.45–7.55; lipid emulsion for severe local anesthetic/bupropion toxicity

— Bidirectional VT (alternating axis), frequent PVCs, AV blocks, atrial tachycardia with block, scooped ST depressions

— Triggers: renal failure, hypokalemia, hypomagnesemia, hypercalcemia, drug interactions (amiodarone, verapamil, quinidine)

— Treat with digoxin-specific Fab fragments; avoid cardioversion if possible (precipitates VF) — use lowest energy if unstable

— Wide-complex, dysrhythmic patterns — correct underlying derangement

— Bradycardia, Osborn (J) waves, then VF — rewarm before defibrillating beyond initial attempts

— Endless-loop tachycardia in dual-chamber pacemakers — apply magnet to convert to asynchronous mode

— Patient tremor, shivering, lead movement can mimic VT — check pulse, look for "marching out" of underlying QRS through artifact

Hyperkalemia:

Sodium-channel blocker toxicity:

Digoxin toxicity:

Severe acidosis or hypoxia:

Hypothermia:

Pacemaker malfunction / pacemaker-mediated tachycardia (PMT):

Artifact:

Step 3 management: A patient on a thiazide with a wide-complex, irregular rhythm and recent vomiting needs immediate K+ and Mg2+ measurement — empiric repletion is reasonable while awaiting labs.

Board pearl: TCA overdose + wide QRS + hypotension = sodium bicarbonate boluses — narrows QRS and is the lifesaving intervention; do not give Class IA/III antiarrhythmics (worsens sodium-channel blockade).

Secondary Prevention and Long-Term Plan

— Survivors of cardiac arrest due to VT/VF without reversible cause

— Sustained VT with structural heart disease

— Syncope with inducible sustained VT on EPS

— Place before discharge unless contraindicated

— Ischemic cardiomyopathy with LVEF ≤30% (NYHA I) or ≤35% (NYHA II–III) ≥40 days post-MI on optimal medical therapy

— Nonischemic cardiomyopathy with LVEF ≤35% and NYHA II–III ≥3 months on GDMT

— HCM with high-risk features (prior arrest, sustained VT, family SCD, syncope, massive LVH ≥30 mm, abnormal BP exercise response, extensive LGE)

— ARVC, LQTS, Brugada, CPVT — risk-stratified by syndrome-specific criteria

— Beta-blockers (metoprolol succinate, carvedilol, bisoprolol) — first-line, reduce SCD risk in HFrEF, post-MI, all channelopathies

— Amiodarone — for breakthrough VT despite ICD; long-term toxicity profile must be weighed

— Sotalol — alternative; QT monitoring required

— Mexiletine — adjunct for LQT3 and refractory VT

— High-intensity statin, ASA, beta-blocker, ACEi/ARB or ARNI, MRA if HFrEF, SGLT2 inhibitor if HFrEF or diabetes

— For recurrent monomorphic VT, recurrent ICD shocks, idiopathic VT (curative for RVOT, fascicular)

— LQTS: avoid QT-prolonging drugs (crediblemeds.org); LQT1 avoid strenuous swimming; LQT2 avoid sudden loud noises

— Brugada: aggressive fever treatment, avoid Na-channel blockers, alcohol binges

— CPVT: exercise restriction

ICD for secondary prevention:

ICD for primary prevention:

Pharmacologic suppression (with or alongside ICD):

Optimal medical therapy for ischemic substrate:

Catheter ablation:

Trigger avoidance:

Step 3 management: Defer ICD ≥40 days after MI and ≥3 months after diagnosis of nonischemic CM — within these windows, use wearable cardioverter-defibrillator (LifeVest) while reassessing EF on optimal therapy.

Board pearl: Beta-blockers reduce SCD across nearly every substrate — post-MI, HFrEF, LQTS, CPVT, HCM. Memorize this universal applicability.

Follow-Up, Monitoring, and Counseling

— Cardiology/EP within 1–2 weeks of discharge

— Device clinic for ICD interrogation at 2–4 weeks, then every 3–6 months (or remote monitoring)

— Primary care within 1 week for medication reconciliation, BP, electrolytes

— Echo at 3 months to reassess LVEF if borderline for ICD

— Amiodarone: baseline TSH, LFTs, CXR, PFTs, ophthalmologic exam; TSH and LFTs every 6 months; CXR annually; PFTs if pulmonary symptoms; ECG for QT

— Sotalol/dofetilide: ECG and electrolytes at each visit; renal function quarterly

— Procainamide (chronic): CBC, ANA; discontinue if drug-induced lupus develops

— Beta-blockers: HR, BP, symptoms of bronchospasm/depression

— Statin: lipid panel at 4–12 weeks then annually; LFTs if symptomatic

— Driving restrictions: post-VT with ICD, no driving for ≥6 months (private), permanent restriction for commercial license; AHA/HRS guidelines

— Activity: resume normal activity per cardiac rehab; competitive sports restriction in inherited channelopathies and HCM (individualized 2020 AHA/ACC guidance)

— ICD living: what a shock feels like, when to call EMS (one shock + symptoms or ≥2 shocks → 911), avoid strong magnets/MRI unless device is MRI-conditional

— Medication adherence — emphasize beta-blocker continuity; abrupt withdrawal precipitates rebound arrhythmia

— Referral for all patients post-MI, post-revascularization, with HFrEF, post-arrest — Class I recommendation

— Improves mortality, functional capacity, depression

— First-degree relatives of patients with inherited channelopathy or cardiomyopathy → ECG, echo, exercise stress, genetic counseling

Post-discharge follow-up cadence:

Monitoring parameters:

Patient counseling:

Cardiac rehabilitation:

Family screening:

Step 3 management: A patient with a new ICD who reports a single appropriate shock and feels well: call EP for device interrogation within 24 hours; ED visit not mandatory unless symptomatic or multiple shocks. Reinforce no driving for the duration recommended.

CCS pearl: On CCS, always order "counsel patient on driving restrictions" and "cardiac rehabilitation referral" before ending a post-VT case — these are gradeable items.

Ethical, Legal, and Patient Safety Considerations

— Discuss benefits (mortality reduction in appropriate candidates) and risks (infection, lead complications, inappropriate shocks, psychological burden)

— Shared decision-making is required by CMS for primary-prevention ICDs — document discussion of alternatives (medical therapy alone, wearable defibrillator) and patient values

— Particular care in elderly or those with limited life expectancy — ICD may not improve quality or quantity of life if competing comorbidities dominate

— Patients or surrogates may request deactivation; this is ethically and legally permissible (analogous to withdrawal of life-sustaining therapy), not euthanasia

— Coordinate with EP, palliative care, and the patient's care goals

— Reprogram to disable shocks while leaving pacing function if pacing-dependent; this is a routine palliative care intervention

— Failure to discuss deactivation in dying patients leads to distressing shocks — a sentinel patient safety issue

— Physicians have an ethical (and in some states legal) duty to counsel against driving after VT/ICD; document the conversation

— State-specific mandatory reporting laws vary — know your state (e.g., California requires reporting lapses of consciousness to DMV)

— Discharge after WCT carries high readmission risk — ensure medication reconciliation, QT-prolonging drug review, electrolyte plan, and timely EP follow-up

— A common Step 3 trap: discharging a patient on amiodarone without arranging TSH/LFT monitoring or warning about pulmonary symptoms

— Sudden death of a young athlete may trigger coroner involvement; preserve tissue for genetic analysis (cardiac autopsy)

— Family must be referred for screening — failure to do so risks preventable death in relatives

— Clarify code status before ICD placement and before any high-risk procedure

— DNR/DNI does NOT automatically mean ICD deactivation — these are separate decisions requiring explicit discussion

Informed consent for ICD:

End-of-life ICD deactivation:

Driving restrictions:

Transition-of-care risks:

Mandatory reporting:

Resuscitation status:

Step 3 management: A hospice patient with a functioning ICD experiencing repeated shocks needs urgent reprogramming or magnet placement — this is a quality-of-dying patient safety priority and a frequent Step 3 ethics vignette.

Board pearl: Disabling an ICD at a patient's request is ethically equivalent to withdrawing any other life-sustaining therapy — it is not physician-assisted death.

High-Yield Associations and Rapid-Fire Facts

VT until proven otherwise: WCT in patient >35 with prior MI/structural heart disease

Brugada criteria → VT if: absence of RS in precordials, RS interval >100 ms, AV dissociation, or VT morphology in V1/V6

Cannon A waves + variable S1 = AV dissociation = VT

Concordance (all precordial leads same polarity) = VT

Extreme axis (northwest) = VT

Capture and fusion beats = VT (pathognomonic when present)

AIVR (50–120 bpm, wide) after STEMI reperfusion = benign, do not treat

Bidirectional VT = digoxin toxicity or CPVT

Torsades = polymorphic VT + long QT → IV magnesium, correct K, withdraw offending drugs

AF + WPW = irregular, polymorphic, very wide, very fast (>250 bpm) → procainamide or cardioversion; avoid ABCD (Adenosine, Beta-blockers, Calcium channel blockers, Digoxin)

Procainamide > amiodarone for stable monomorphic VT (PROCAMIO trial)

Amiodarone preferred in HF/reduced EF and renal failure

Lidocaine preferred in ischemia-driven VT

Sodium bicarbonate for TCA/sodium-channel blocker toxicity with wide QRS

Calcium gluconate for hyperkalemia-induced WCT

Digoxin Fab for digoxin toxicity

ICD primary prevention: EF ≤35% with NYHA II–III on GDMT ≥3 months, ≥40 days post-MI

Wearable defibrillator bridges the 40-day post-MI / 3-month nonischemic CM window

Idiopathic VT subtypes: RVOT (LBBB + inferior axis, beta-blocker/ablation), fascicular (RBBB + LAD, verapamil-sensitive)

LQT1: exercise (especially swimming); LQT2: auditory startle; LQT3: sleep

Brugada triggers: fever, sodium-channel blockers, alcohol, cocaine

CPVT: exercise/emotion → bidirectional VT, beta-blockers ± flecainide

Driving restriction: 6 months after symptomatic VT or appropriate ICD shock (private license)

Amiodarone toxicity mnemonic — "PHOTOS": Pulmonary fibrosis, Hepatitis, Ophthalmologic (corneal/optic), Thyroid (hyper/hypo), Optic neuropathy, Skin (blue-gray)

Sotalol/dofetilide require inpatient initiation with continuous QT monitoring

Step 3 management: When you see "wide, fast, irregular, bizarre QRS in a young patient" → think AF with WPW and reach for procainamide or cardioversion, never adenosine or diltiazem.

Board Question Stem Patterns

— 68-year-old man with prior anterior MI presents with palpitations and lightheadedness; HR 170, BP 100/60, regular WCT on ECG with AV dissociation

— Answer: Sustained monomorphic VT → IV procainamide (or amiodarone), prepare for synchronized cardioversion if deteriorates; admit, echo, EP consult, ICD evaluation

— Patient with WCT, BP 70/40, altered, cool extremities

— Answer: Synchronized cardioversion 100 J biphasic immediately, not adenosine, not amiodarone first

— Young patient with palpitations, irregular WCT >250 bpm, bizarre QRS morphology varying beat to beat, history of WPW

— Answer: Procainamide or synchronized cardioversion; never adenosine, beta-blockers, calcium channel blockers, or digoxin

— Patient on azithromycin + ondansetron + methadone, develops polymorphic VT with long QT

— Answer: IV magnesium 2 g, correct K to >4, withdraw offending agents, overdrive pacing if recurrent

— Dialysis patient missed sessions, presents with sine-wave wide-complex rhythm

— Answer: IV calcium gluconate first, then insulin/glucose, albuterol, bicarbonate, urgent dialysis

— Elderly woman on digoxin + furosemide with bidirectional VT, nausea, yellow vision

— Answer: Digoxin-specific Fab fragments, correct K and Mg; avoid cardioversion if possible

— Patient post-thrombolysis develops regular wide-complex rhythm at 85 bpm, hemodynamically stable

— Answer: AIVR — observe, no antiarrhythmic (reperfusion rhythm)

— Patient 6 months post-MI on optimal GDMT, repeat echo shows EF 28%, NYHA II

— Answer: Primary-prevention ICD indicated

— Young swimmer collapses; resuscitated; QTc 510 ms on ECG

— Answer: LQT1, beta-blocker (nadolol), avoid QT drugs, family screening, swimming restriction

— Hospice patient with ICD getting repeated shocks at end of life

— Answer: Deactivate ICD shock function per patient/family wishes — ethically appropriate

Stem 1 — Classic VT vignette:

Stem 2 — Unstable WCT:

Stem 3 — Pre-excited AF:

Stem 4 — Torsades:

Stem 5 — Hyperkalemia mimic:

Stem 6 — Digoxin toxicity:

Stem 7 — AIVR after STEMI:

Stem 8 — ICD candidacy:

Stem 9 — Inherited:

Stem 10 — Ethics:

Board pearl: The single most tested Step 3 trap is giving adenosine, verapamil, or diltiazem to AF with WPW — recognize the irregular, bizarre, very fast WCT and reach for procainamide or shock.

One-Line Recap

Wide-complex tachycardia is VT until proven otherwise — stabilize first (synchronized cardioversion if unstable, procainamide or amiodarone if stable), correct reversible causes (electrolytes, ischemia, toxins), and never give AV-nodal blockers to irregular pre-excited tachycardias.

Recognition shortcut: Regular monomorphic WCT + prior MI or structural heart disease = VT; AV dissociation, capture/fusion beats, concordance, or extreme axis seals the diagnosis

Acute management algorithm: Pulseless → defibrillate per ACLS; unstable with pulse → synchronized cardioversion 100 J; stable monomorphic → procainamide (or amiodarone if reduced EF); polymorphic with long QT → IV magnesium; irregular pre-excited (AF + WPW) → procainamide or cardioversion, never ABCD (Adenosine, Beta-blockers, Calcium channel blockers, Digoxin)

Reversible causes to chase in parallel: Hyperkalemia (calcium gluconate), TCA/sodium-channel toxicity (sodium bicarbonate), digoxin toxicity (Fab fragments), hypomagnesemia, ischemia, hypoxia, drug-induced QT prolongation

Long-term plan: Echo + ischemia workup + EP consult before discharge; ICD for survivors of unexplained VT/VF and for primary prevention in HFrEF (EF ≤35% on GDMT, ≥40 days post-MI or ≥3 months nonischemic CM); beta-blocker baseline, statin/ACEi/SGLT2 if ischemic substrate; counsel on driving restrictions (6 months post-event), cardiac rehab, family screening for inherited syndromes, and end-of-life ICD deactivation discussions when appropriate

Step 3 management: When the rhythm is fast, wide, irregular, and bizarre in a young patient — think pre-excited AF, reach for procainamide or the defibrillator, and walk away from the AV node.