VT vs SVT: The Emergency ECG Decision Every Doctor Must Master

Arrhythmias Life-Threatening ECG Emergency Medicine Critical Care    ★★★★ Advanced  |  20 min read  |  Published: June 13, 2026

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It's 2:47 AM.

You're the only doctor in the ED. The triage nurse calls you urgently to Bay 3.

"58-year-old male. Known heart failure. Came in with palpitations and nearly passed out at home. HR is 182. BP is 94 over 60."

You walk in. He's pale, diaphoretic, anxious. Talking to you — but barely. The 12-lead ECG is already printing.

You look at it.

Wide. Regular. Fast.

Your intern looks over your shoulder: "Could this be SVT with aberrancy? Should I give adenosine?"

You have 45 seconds to decide. The right answer keeps this man alive. The wrong answer could kill him.

⛔ STOP — Before you scroll down. Look at the ECG findings below and make your diagnosis. Then continue reading.

⚡ THE CASE ECG — Wide Complex Tachycardia — What is your diagnosis?

12-lead ECG  |  Rate: 182 bpm  |  QRS: 160 ms  |  Wide complex tachycardia  |  Analyse before scrolling

The ECG — Read It Now

Parameter	Finding
Rate	182 bpm
Rhythm	Regular
QRS duration	160 ms
Axis	Northwest (negative I and aVF)
Morphology	LBBB-like, atypical
Concordance	Positive — all chest leads positive
P Waves	Marching independently, different rate
Fusion Beat	One visible in Lead II
Capture Beat	One visible — single narrow QRS

What is your diagnosis?   A) SVT with LBBB aberrancy   B) Ventricular tachycardia   C) AF with aberrancy   D) Antidromic AVRT

✓ The Answer: Ventricular Tachycardia

Three features alone are pathognomonic: AV dissociation, fusion beats, positive concordance. The diagnosis is made.

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1. Understanding Wide Complex Tachycardia

Defined as: heart rate > 100 bpm AND QRS duration > 120 ms. Four causes: VT (most common), SVT with functional aberrancy, SVT with pre-existing BBB, antidromic AVRT in WPW.

In adults >35 with structural heart disease — VT in 80% of WCT. In all-comers — VT in 70%.

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2. Physiology

Normal: SA → AV → His → Purkinje → both ventricles → narrow QRS. VT: focal ventricular origin → slow myocardial spread → wide bizarre QRS. SVT with aberrancy: supraventricular origin but one bundle branch blocked → recognisable BBB pattern. VT looks bizarre; SVT looks like BBB.

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3. The Brugada Algorithm

Stop at the first YES:

Q1: No RS in ALL precordial leads?     YES --> VT Q2: RS interval >100 ms in ANY lead?   YES --> VT Q3: AV dissociation?                    YES --> VT Q4: Morphology criteria?                YES --> VT All NO --> SVT with aberrancy Sensitivity: 98.7% | Specificity: 96.5%

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4. Vereckei aVR Criterion

One lead only: Initial R wave in aVR, or r/q >40ms, or notch on descending limb, or Vi/Vt ratio ≤1 — any one = VT. Bedside: any initial positive deflection in aVR — strongly suggests VT.

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5. VFCAN Checklist

V — Very wide QRS (>160 ms)
F — Fusion / Capture beats (PATHOGNOMONIC)
C — Concordance (all V1–V6 same direction)
A — AV Dissociation (PATHOGNOMONIC)
N — Northwest axis (negative I and aVF)

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6. The Golden Rule

"In the absence of strong evidence for SVT with aberrancy, treat ALL WCT as VT." — Brugada et al., Circulation 1991

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7. The Verapamil Danger

⚠ NEVER give verapamil in unconfirmed WCT
If patient has VT: verapamil causes vasodilation + negative inotropy → cardiac collapse. Adenosine is safe in both VT and SVT. Use it.

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8. Management

Unstable (BP <90, altered GCS, pulmonary oedema): Synchronised DC cardioversion immediately. Sedate first. Do not wait for algorithm.

Stable VT: IV Amiodarone 300 mg over 20–60 min.   Stable SVT: Adenosine 6 mg IV bolus.   Still uncertain? Treat as VT and call senior.

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9. The 5 Forms of VT

Form	Key Feature	Weight
Classic Monomorphic VT	Regular, wide, fast	Suggestive
VT + AV Dissociation	P waves marching independently	PATHOGNOMONIC ✓
VT + Fusion/Capture	Hybrid or narrow QRS interrupts	PATHOGNOMONIC ✓
Torsades de Pointes	Twisting polymorphic	IV Mg — NOT amiodarone
Positive Concordance	All V1–V6 positive	Brugada Q1 ✓

⚡ ECG Visual Gallery — Recognise All 5 Forms of VT

Interactive ECG strips drawn to scale  |  25 mm/s  |  Each strip annotated with key diagnostic features

1

Classic Monomorphic Ventricular Tachycardia

Lead II Rhythm Strip  |  Rate ~180 bpm  |  QRS 160 ms  |  Regular  |  No P waves visible

VT complex (broad, notched)

QRS width annotation (160 ms)

Rate ~180 bpm. Fast — but speed alone never confirms or excludes VT.

QRS Width 160 ms (4 small squares). Far exceeds 120 ms threshold.

Morphology Broad, slurred, notched upstroke. Discordant T wave.

Regularity Perfectly regular RR intervals — hallmark of monomorphic VT.

Teaching Point: This is the most common presentation at 3 AM. Regular, fast, wide. The QRS is more than 4 small squares wide with slurring, notching, and a discordant T wave. The depolarisation wavefront did not travel through the His-Purkinje system — it came from inside the ventricle. That means VT.

2

Ventricular Tachycardia — AV Dissociation

Lead II  |  VT rate ~160 bpm  |  P waves at ~75 bpm marching independently  |  PATHOGNOMONIC for VT

VT complex

P wave (independent atrial activity)

AV Dissociation P waves (blue) march at ~75 bpm, completely independent of QRS at 160 bpm.

Diagnostic Value PATHOGNOMONIC for VT. One finding alone ends the differential. No algorithm needed.

Teaching Point: The atria and ventricles are living separate lives. The sinus node fires normally at 75 bpm — you can see the P waves in the ST segments and T waves. But none of those P waves are conducting. This is the definition of AV dissociation, and it is pathognomonic for ventricular tachycardia. If you see this — stop. The diagnosis is made.

3

Ventricular Tachycardia — Fusion Beat & Capture Beat

Lead II  |  Rate ~150 bpm  |  Both pathognomonic features of VT visible in a single strip

VT complex (broad)

Fusion beat (F) — hybrid morphology

Capture beat (C) — narrow, normal QRS

Fusion Beat (F) VT focus and sinus impulse activate ventricles simultaneously — hybrid QRS: narrower than VT, wider than normal.

Capture Beat (C) Sinus impulse arrives at exactly the right moment — single narrow QRS interrupting the VT rhythm.

Diagnostic Weight Either finding alone is pathognomonic for VT. Both together = zero diagnostic doubt.

Teaching Point: Think of two electrical grids. A fusion beat happens when both grids fire simultaneously — hybrid QRS. A capture beat happens when the sinus grid briefly wins — single normal narrow QRS. Both are proof that the VT generator is ventricular, not supraventricular.

4

Torsades de Pointes — Polymorphic Ventricular Tachycardia

Lead II  |  Irregular  |  QRS complexes twist around the isoelectric line  |  Preceding QTc: 590 ms

Polymorphic VT complexes (varying axis & amplitude)

Polymorphic QRS Each complex has a different axis and amplitude. No two QRS complexes look identical.

Twisting Pattern Complexes appear to twist around the isoelectric baseline — positive group, then negative group.

QTc Context Occurs in the setting of QTc prolongation (>500 ms). Triggered by R-on-T phenomenon.

⚠ Critical Danger: Torsades de Pointes is managed DIFFERENTLY from monomorphic VT. Amiodarone prolongs QT — do NOT give it. First-line: IV Magnesium Sulphate 2g over 10–15 minutes. Correct K+ to >4.5 mmol/L. Stop all QT-prolonging drugs.

5

Ventricular Tachycardia — Positive Concordance (Precordial Leads V1–V6)

All 6 precordial leads show tall positive R waves  |  No RS transition  |  Answers Brugada Question 1 = VT

VT complexes (all leads positive — concordance)

Expected normal RS transition zone (absent)

Positive Concordance All leads V1–V6 show tall, predominantly positive QRS complexes.

No RS Transition Normally V1–V2 are negative, V5–V6 positive, transition in V3–V4. In concordance, this transition is absent.

Brugada Algorithm Answers Q1 (no RS in ALL precordial leads) with YES → VT. Diagnosis made at Step 1.

Teaching Point: In normal conduction, the Purkinje system creates a bidirectional wavefront — V1 negative, V6 positive, transition in between. Concordance means the wavefront moves consistently in one direction toward all precordial leads. This can only happen from a focal abnormal ventricular source. Brugada Q1 is answered. It's VT.

REF

Bedside Reference — 5 Forms of VT at a Glance

Quick identification guide

Form of VT	Key ECG Feature	Diagnostic Weight	Critical Management
Classic Monomorphic VT	Regular, wide (>120 ms), fast	Highly suggestive	Amiodarone / Cardiovert
VT + AV Dissociation	P waves march independently	PATHOGNOMONIC ✓	Confirms VT
VT + Fusion/Capture	Hybrid or narrow QRS interrupts	PATHOGNOMONIC ✓	Confirms VT
Torsades de Pointes	Irregular, polymorphic, twisting	Diagnostic morphology	⚠ IV Mg — NOT amiodarone
VT + Positive Concordance	All V1–V6 positive, no RS transition	Brugada Q1 = VT ✓	Confirms VT

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10. Bedside Pearls

The 30-Second Takeaway: WCT = VT until proven otherwise. Unstable: cardiovert now. Stable: Brugada algorithm. AV dissociation, fusion/capture beats, concordance, northwest axis all confirm VT. Never verapamil. Adenosine is safe.

High-Yield Exam Points

1. VT accounts for ~70% of all WCT in adults
2. AV dissociation, fusion/capture beats = pathognomonic
3. Brugada sensitivity 98.7%
4. Unstable WCT = synchronised cardioversion
5. Stable VT = amiodarone 300 mg IV
6. Adenosine safe; verapamil dangerous
7. Northwest axis = VT
8. Concordance = VT
9. Torsades = IV magnesium, not amiodarone

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Test Yourself — 5 MCQs

Q1. A 62 yo man, ischaemic cardiomyopathy, WCT 176 bpm, BP 100/70. P waves marching independently. Diagnosis?

A) SVT with LBBB   B) Ventricular tachycardia   C) AF with aberrancy   D) Antidromic AVRT

✓ B. AV dissociation is pathognomonic for VT.

Q2. Most dangerous drug in VT misdiagnosed as SVT?

A) Adenosine   B) Amiodarone   C) Verapamil   D) Metoprolol

✓ C. Verapamil causes cardiac collapse in VT.

Q3. RS interval 130 ms in V4. Diagnosis?

A) SVT with aberrancy   B) Further analysis needed   C) VT   D) Inconclusive

✓ C. Brugada Q2: RS >100 ms = VT.

Q4. V1–V6 all positive, no RS transition. What is this?

A) RBBB — SVT   B) Normal variant   C) Positive concordance — VT   D) Posterior STEMI

✓ C. Brugada Q1 — VT.

Q5. 74 yo dilated cardiomyopathy, WCT 200 bpm, BP 68/40, GCS 13. Management?

A) Adenosine   B) Amiodarone   C) 12-lead + cardiology   D) Synchronised DC cardioversion

✓ D. Cardiovert immediately.

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Viva Questions

Viva 1: Walk me through the Brugada algorithm.
Answer: Q1: no RS all leads → VT. Q2: RS >100ms → VT. Q3: AV dissociation → VT. Q4: morphology criteria → VT. All no → SVT with aberrancy. Sensitivity 98.7%.

Viva 2: Colleague suggests verapamil for WCT. Response?
Answer: Not until VT excluded. If VT — verapamil causes collapse. Adenosine is safe and diagnostic.

Viva 3: What are fusion and capture beats?
Answer: Both pathognomonic for VT. Fusion: sinus + ventricular foci fire together → hybrid QRS. Capture: sinus briefly wins → single narrow QRS. Both prove independent ventricular focus.

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Resolution — Back to Bay 3

AV dissociation ✓. QRS 160 ms. Northwest axis. Positive concordance. Fusion beat present.

Turn to intern: "This is VT. Get the crash cart. I'm sedating and cardioverting."

Cardiovert 150J biphasic. Sinus rhythm restores. BP to 118/76.

"How did you know so fast?" — You hand them this article.

Evidence Base

• Brugada P et al. Circulation. 1991;83(5):1649–1659.
• Vereckei A et al. Heart Rhythm. 2008;5(1):89–98.
• Wellens HJ et al. Am J Med. 1978;64:27–33.
• ESC Guidelines 2015 — Ventricular Arrhythmias.
• AHA/ACC/HRS Guideline 2017.

© Emergency Medicine & Critical Care Educational Platform  |  Published: June 13, 2026