Wide-Complex Tachycardia, Torsades & Inherited Arrhythmia Syndromes
VT until proven otherwise, then the torsades and channelopathy traps
Recognizing VT in a wide-complex tachycardia
Definition. A wide-complex tachycardia (WCT) has a QRS of at least 120 ms and a rate above 100 bpm. Ventricular tachycardia accounts for about 80% of all WCTs and more than 90% in patients with prior MI or other structural heart disease, so a WCT is treated as VT until proven otherwise. Normal blood pressure and a comfortable patient do not argue against VT.
Differential. The alternatives are SVT conducted with a bundle branch block (aberrancy), preexcited tachycardia over an accessory pathway, and ventricular pacing. Metabolic and toxic mimics also widen the QRS: hyperkalemia (peaked T waves, then a sine wave) needs IV calcium, and tricyclic or other sodium-channel-blocker toxicity (terminal R in aVR) needs IV sodium bicarbonate rather than procainamide.
| Feature | Favors VT | Favors SVT with aberrancy |
|---|---|---|
| History | Prior MI, low EF, cardiomyopathy | Young, structurally normal heart, long history of SVT |
| Atrial activity | AV dissociation; fusion and capture beats (diagnostic) | 1:1 P–QRS relationship |
| QRS | >160 ms, extreme northwest axis, precordial concordance | Typical RBBB or LBBB pattern matching an old baseline ECG |
| Bedside | Cannon a waves, variable intensity of S1 | Regular neck veins; may stop with vagal maneuvers or adenosine |
Idiopathic VT. A minority of VT arises in structurally normal hearts: outflow-tract VT (LBBB pattern, inferior axis, often exercise-provoked) and fascicular VT (RBBB pattern with left axis deviation). Both carry a good prognosis and are often cured by ablation; fascicular VT is the rare verapamil-sensitive VT, recognized only by specialists after the diagnosis is secure.
Acute management by stability
- No pulsePulseless VT or VF → CPR, unsynchronized defibrillation and ACLS (epinephrine, amiodarone or lidocaine).
- Pulse but unstableHypotension, altered mentation, ischemic chest pain, acute heart failure or shock → immediate synchronized cardioversion (about 100 J biphasic to start), with sedation if time allows. Polymorphic VT cannot be synchronized and is defibrillated.
- Stable monomorphic12-lead ECG, correct K and Mg, then IV amiodarone (150 mg over 10 minutes) or procainamide; sotalol and lidocaine are alternatives.
- Drugs failElective synchronized cardioversion, then look for ischemia and structural disease and refer to electrophysiology.
Drug cautions. Procainamide and sotalol are avoided when the QT is prolonged, and procainamide in severe heart failure. Adenosine may be tried only for a regular, monomorphic WCT thought to be SVT; it rarely terminates VT and is dangerous in an irregular WCT.
Never give IV verapamil or diltiazem for a wide-complex tachycardia: in VT, vasodilation plus negative inotropy can cause collapse and VF.
Preexcited atrial fibrillation. An irregular, very fast WCT (often 250–300 bpm) with beat-to-beat variation in QRS width suggests AF conducting over an accessory pathway in WPW. AV-nodal blockers (calcium channel blockers, β-blockers, digoxin, adenosine, and IV amiodarone) divert conduction down the pathway and can precipitate VF. Use procainamide (or ibutilide) if stable and cardioversion if unstable; ablation of the pathway is definitive.
Polymorphic VT with a normal QT. When the QT between runs is normal, polymorphic VT is usually acute ischemia rather than torsades. Defibrillate if sustained, give IV amiodarone or lidocaine plus a β-blocker, and proceed to urgent coronary angiography and revascularization; magnesium alone will not fix it. Three or more VT/VF episodes in 24 hours (electrical storm) call for β-blockade, amiodarone, sedation and ablation.
Torsades de pointes and the acquired long QT
Mechanism. Prolonged repolarization allows early afterdepolarizations during phase 2–3 of the action potential. An afterdepolarization that reaches threshold fires an R-on-T PVC, often after a short-long-short sequence, launching polymorphic VT whose axis twists around the baseline. Most runs self-terminate, but sustained torsades degenerates into VF.
Risk factors. QTc above 500 ms (or a rise of more than 60 ms from baseline), hypokalemia, hypomagnesemia, hypocalcemia, bradycardia or pauses, female sex, structural heart disease, and stacking several QT-prolonging drugs, especially with diuretic-induced hypokalemia.
- Antimicrobials: macrolides, fluoroquinolones, azole antifungals
- Psychiatric and opioid drugs: haloperidol and other antipsychotics, TCAs, methadone
- Antiemetics: ondansetron
- Antiarrhythmics: class IA (quinidine, procainamide, disopyramide) and class III (sotalol, dofetilide, ibutilide; amiodarone prolongs QT but rarely causes torsades)
Treatment. Give 2 g of IV magnesium sulfate even when the serum magnesium is normal, raise potassium to 4.5–5 mEq/L, and stop every offending drug. For recurrent, pause-dependent torsades, shorten the QT by increasing the heart rate with transvenous overdrive pacing or an isoproterenol infusion. Sustained or pulseless torsades is defibrillated. Amiodarone and procainamide lengthen the QT further and are wrong here.
Isoproterenol helps acquired, pause-dependent torsades but is avoided in congenital long QT, where adrenergic surges are the trigger; pace those patients instead.
Inherited arrhythmia syndromes
| Syndrome | Genetics | ECG clue | Trigger | Key therapy |
|---|---|---|---|---|
| Brugada | SCN5A loss of function; autosomal dominant | Coved ST elevation ≥2 mm with T inversion in V1–V2 | Rest, sleep, fever, sodium-channel blockers | Antipyretics, avoid triggers; ICD if syncope or arrest; quinidine |
| LQT1 | KCNQ1 (IKs ↓) | Long QTc | Exercise, especially swimming | Nonselective β-blocker |
| LQT2 | KCNH2/hERG (IKr ↓) | Long QTc | Loud noise, emotion, postpartum | Nonselective β-blocker |
| LQT3 | SCN5A gain of function (late Na current ↑) | Long QTc | Rest or sleep | β-blocker ± mexiletine |
| ARVC | Desmosomal (plakophilin-2); usually dominant | T inversion V1–V3, epsilon waves, LBBB-morphology VT | Exertion | Exercise restriction, β-blocker, ablation, ICD if high risk |
| CPVT | RYR2 (dominant) or CASQ2 (recessive) | Normal at rest; bidirectional VT on exercise | Exercise, emotion | Nadolol, add flecainide; ICD for arrest or refractory events |
Brugada syndrome. Reduced sodium current in the RV outflow tract produces the type 1 pattern, a pseudo-RBBB with coved ST elevation in V1–V2 that is a classic STEMI mimic. It typically affects young men with structurally normal hearts, with VF at rest or during sleep, and underlies many sudden unexplained nocturnal deaths of young Southeast Asian men. Fever, class IC drugs (flecainide, propafenone), TCAs, cocaine, lithium and heavy alcohol unmask the pattern and provoke VF; a procainamide or ajmaline challenge is diagnostic. Treat fever promptly, avoid triggers, and implant an ICD after arrhythmic syncope or aborted sudden death; quinidine suppresses recurrent VF. An asymptomatic, drug-induced pattern alone is managed conservatively.
Congenital long QT. Suspect it with exertional or startle-induced syncope, events misdiagnosed as seizures, unexplained drowning, or a family history of sudden death; a QTc of 480 ms or more on repeated ECGs supports the diagnosis. Nadolol or propranolol is first-line for nearly all patients and protects best in LQT1, together with avoidance of QT-prolonging drugs and potassium and magnesium repletion. An ICD is added for cardiac arrest survivors or recurrent syncope despite β-blockade; left cardiac sympathetic denervation and, in LQT3, mexiletine are adjuncts. Romano-Ward syndrome is autosomal dominant with normal hearing; Jervell and Lange-Nielsen syndrome (autosomal recessive, KCNQ1 or KCNE1) adds congenital sensorineural deafness.
ARVC. Fibrofatty replacement of the RV myocardium causes right precordial T inversion, epsilon waves (a small notch just after the QRS in V1–V3) and VT with LBBB morphology, classically with exertion in a young athlete. Cardiac MRI shows RV dilation, dyskinesia and fat. Because exercise accelerates the disease, competitive and endurance sports are restricted. HCM, by contrast, shows LVH with septal Q waves.
CPVT. Mutant ryanodine receptors (RYR2) or calsequestrin (CASQ2) leak calcium from the sarcoplasmic reticulum under adrenergic stress, causing syncope or sudden death with exercise or emotion in children and teens. Resting ECG and echocardiogram are normal, so exercise testing is key. Bidirectional VT has two classic causes: CPVT and digoxin toxicity.
Implantable cardioverter-defibrillators
Secondary prevention. Survivors of VF or hemodynamically unstable VT, and patients with sustained VT and structural heart disease, receive an ICD when no completely reversible cause is found; antiarrhythmic drugs alone are inferior. VF within the first 48 hours of an acute MI, or arrest from severe hyperkalemia or drug toxicity, is treated by correcting the cause, not with an ICD.
Primary prevention. An ICD is offered for LVEF ≤35% with NYHA class II–III symptoms despite at least 3 months of guideline-directed therapy (ischemic or nonischemic), or LVEF ≤30% in NYHA class I after MI, when survival beyond 1 year is expected. Stunned myocardium often recovers after MI, so EF is re-measured after a mandatory wait; a wearable defibrillator can bridge high-risk patients.
A subcutaneous ICD avoids transvenous leads but cannot provide bradycardia or antitachycardia pacing, so it suits young patients without pacing needs; channelopathy patients with syncope or arrest are ICD candidates regardless of EF.