Differentials for wide complex tachy
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I have solid material from Braunwald's, Rosen's, and Harrison's. Let me also grab the Tintinalli differential section and look for the Braunwald's figure of the WCT management algorithm.
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I now have comprehensive content from four major textbooks. Here is the full differential:
Differentials for Wide-Complex Tachycardia (WCT)
Definition: Any tachycardia with QRS ≥ 120 ms (0.12 s).
The Core Categories
1. Ventricular Origin (~80% of cases)
| Diagnosis | Key Features |
|---|---|
| Ventricular tachycardia (VT) — monomorphic | Most common cause; AV dissociation, fusion beats, concordance |
| VT — polymorphic (including TdP) | Irregular, twisting axis; may be triggered by long QT or ischemia |
| Bundle branch re-entry VT | Usually LBBB morphology; seen in dilated cardiomyopathy |
| Fascicular tachycardia | Relatively narrow WCT (~120–140 ms), RBBB + left axis deviation; typically in young patients with no structural disease |
2. SVT with Aberrant Conduction
| Diagnosis | Key Features |
|---|---|
| SVT + rate-related (functional) BBB | BBB appears only at fast rates |
| SVT + pre-existing BBB | Bundle branch block present at baseline |
| SVT + antiarrhythmic-induced BBB | e.g., flecainide, propafenone |
3. Accessory Pathway–Mediated
| Diagnosis | Key Features |
|---|---|
| Antidromic AVRT | Regular; antegrade conduction down the accessory pathway; maximally pre-excited QRS |
| AF with preexcitation (WPW) | Irregular, rapid (can exceed 250 bpm), variable QRS width; potentially lethal |
| Atrial flutter/tachycardia with preexcitation (bystander AP) | Regular WCT; AP conducts but is not part of the reentrant circuit |
4. Metabolic / Toxic Causes
| Diagnosis | Key Features |
|---|---|
| Hyperkalemia | Sinusoidal / bizarre WCT; peaked T waves, absent P waves, broad QRS |
| Sodium channel blocker toxicity | TCAs, flecainide, cocaine; broad QRS, R in aVR, rightward axis |
5. Ventricular Pacing
- Paced rhythm with a wide QRS can mimic VT, particularly pacemaker-mediated tachycardia.
Clues Favouring VT
| Feature | Details |
|---|---|
| AV dissociation | Most specific sign (P waves march through at a different rate) |
| Fusion beats / capture beats | Pathognomonic for VT |
| Concordance | Negative concordance (all precordial leads negative) = strongly VT; positive concordance also usually VT |
| QRS > 160 ms (or > 140 ms with RBBB pattern) | Favours VT |
| No RS complex in any precordial lead | Brugada criterion #1 — VT |
| RS nadir > 100 ms | Brugada criterion #2 — VT |
| aVR criteria | Initial R wave, initial q/r > 40 ms, or notching on downstroke → VT |
| Age + structural heart disease | Prior MI or cardiomyopathy makes VT overwhelmingly more likely |
Clues Favouring SVT with Aberrancy
- Typical RBBB or LBBB morphology (narrow initial deflection, triphasic pattern)
- Identical QRS to a known aberrantly conducted sinus beat on prior ECG
- Young patient, no structural heart disease
- Irregular WCT → think AF with aberrancy or AF with preexcitation (WPW)
- Terminates with adenosine
The Clinical Bottom Line
Treat any new WCT as VT until proven otherwise. Hemodynamic stability does NOT exclude VT — a significant proportion of VT patients remain stable. Misdiagnosing VT as SVT and giving an AV nodal blocker (verapamil, diltiazem) can be fatal, especially in the setting of WPW + AF.
Sources: Braunwald's Heart Disease (Table 65.2); Rosen's Emergency Medicine, 9th ed.; Goldman-Cecil Medicine; Harrison's Principles of Internal Medicine, 22nd ed.; Tintinalli's Emergency Medicine
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