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EMA Cited · Cardiology · Arrhythmia

Wide-complex tachycardia

Updated Oct 29, 2026Adults · ED management19 sources · 13 in PubMed2 figuresResuscitation Council UK 2025 (ERC)

Bottom line

  • Life-threatening features mean a synchronized shock now: shock, syncope with severe or ongoing hypotension, myocardial ischemia, severe heart failure, or just after ROSC.1,2
  • Treat a regular wide-complex tachycardia as VT until proven otherwise. A history of myocardial infarction or heart failure predicted VT with over 95% positive predictive value, and no history feature reliably predicted SVT.3,4
  • Never give verapamil to an undifferentiated wide-complex tachycardia. In one series, VT was misread as SVT in 39% of episodes, and every patient with misread VT who got verapamil deteriorated.5
  • For stable monomorphic VT, procainamide beat amiodarone in the only randomized comparison: fewer major cardiac adverse events (9% vs 41%) and more terminations within 40 minutes (67% vs 38%).6
  • Adenosine is a reasonable test only for a regular, monomorphic rhythm without pre-excitation. 90% of SVTs responded and 2% of VTs did, with no serious adverse events.1,7

First minutes

  1. Check for a pulse. No pulse: this is pulseless VT, so follow the cardiac arrest algorithm and defibrillate.1
  2. ABCDE. Monitor the ECG, blood pressure and SpO₂, record a 12-lead ECG, give oxygen if SpO₂ is below 94%, get IV access, and look for reversible causes.1
  3. Look for life-threatening features: shock (for example, systolic BP under 90 mm Hg with signs of poor perfusion), syncope, heart failure with pulmonary edema or raised JVP, or myocardial ischemia.1
  4. Unstable: synchronized cardioversion, up to 3 attempts, with sedation or anesthesia if the patient is conscious.1,2
  5. Stable: decide whether the QRS is regular and monomorphic, then follow the stable pathway below. Get expert help early.1
FIG 1 · Decision flowCited
  1. Wide (QRS ≥ 0.12 s) and fast, with a pulse. Monitor, record a 12-lead ECG, get IV access, give oxygen if SpO₂ < 94%.1 No pulse: cardiac arrest algorithm.1
  2. Shock, syncope with hypotension, ischemia, severe heart failure, or just after ROSC?
    Yes
    Synchronized shock, up to 3 attempts; 120–150 J first for VT. Sedate if conscious.1
    Still unstable: amiodarone 300 mg IV over 10–20 min or procainamide 10–15 mg/kg (max 1 g) over 20 min, then shock again.1
  3. No: stable
    Is the QRS irregular?
    Yes
    AF with pre-excitation: procainamide or cardioversion.1
    Polymorphic VT with a long QT: magnesium 8 mmol IV over 10 min. Avoid amiodarone. Consider isoprenaline or pacing to raise the rate.1
    Other irregular rhythms: the algorithm does not cover every case, so get expert help.1
  4. No: regular
    Treat it as VT unless proven otherwise. Prior MI or heart failure makes VT very likely.3,4 No verapamil or diltiazem.5
  5. Known or suspected SVT with aberrancy, and no pre-excitation?
    Yes
    Adenosine 6 mg rapid IV, then 12 mg, then 18 mg.1 Known SVT: vagal maneuvers first.1
    A response points to SVT; no response makes VT likely.7 If it fails, treat as VT.1
  6. No, or no response
    Is sedation for cardioversion too risky?
    Yes
    Procainamide 10–15 mg/kg IV over 20 min. Stop for hypotension or QRS widening of 50%.1,8
    Procainamide unavailable or contraindicated: amiodarone 300 mg IV over 10–60 min, then 900 mg over 24 h.1
  7. No
    Synchronized cardioversion under sedation, 120–150 J first, stepping up if needed.1 US guidance also allows drugs first in stable patients; see below.9,10
  8. Arrhythmia or features persist: get expert help. Look for ischemia and structural heart disease.1
FIG 1Wide-complex tachycardia with a pulse. Drawn for this page from the Resuscitation Council UK 2025 guideline and tachyarrhythmia algorithm, and the studies cited below. Each box carries its own citations.1,2

VT or SVT with aberrancy?

A regular wide-complex tachycardia can be VT, SVT with a bundle branch block, SVT slowed by a metabolic problem (hyperkalemia, sodium channel blockade, severe acidosis), antidromic AVRT in Wolff-Parkinson-White syndrome, or a paced rhythm.4 The ECG cannot always tell them apart.4

Favors VTFavors SVT with aberrancy
Prior MI, heart failure or recent angina (positive predictive value > 95%)3Old ECGs with the same bundle branch block morphology4
Age over 35 (sensitivity 92%, positive predictive value 85%)3Old ECGs showing pre-excitation4
AV dissociation, capture beats or fusion beats4Past episodes stopped by adenosine or vagal maneuvers4
Precordial concordance (all positive or all negative)4A typical RBBB or LBBB pattern4
QRS > 160 ms, or a northwest axis4—

No history feature strongly predicted SVT. Age 35 or under was the best, with a positive predictive value of only 70%.3

12-lead ECG of a regular wide-complex tachycardia with tall broad complexes in the precordial leads, labelled ventricular tachycardia
FIG 2Ventricular tachycardia on a 12-lead ECG. A regular, very wide-complex tachycardia, labelled ventricular tachycardia by its author. The tall, broad complexes in V1–V3 do not look like a typical bundle branch block.James Heilman, MD · Wikimedia Commons · CC BY-SA 3.0

ECG algorithms

  • Brugada criteria, in order: no RS complex in any precordial lead; an RS interval over 100 ms; AV dissociation; then VT morphology in V1–V2 and V6. Any yes means VT.4
  • Lead aVR (Vereckei): a dominant initial R wave in aVR points to VT.4
  • None is good enough to rule VT out. In 3,966 patients across 14 studies, the algorithms pooled to 89% sensitivity and 71% specificity for VT.11
  • In a head-to-head comparison of 260 tracings, all five methods had only moderate accuracy. Newer methods were no better than the Brugada algorithm (accuracy 77.5%).12
Why it matters

In 46 emergency episodes, every SVT with aberrancy was diagnosed correctly, but 15 of 38 VTs (39%) were called SVT. AV dissociation was visible in 73% of the misread ECGs. Verapamil was given in 13 of those 15 episodes, and all 13 deteriorated.5

Treatment

TreatmentAdult doseUse forNotes
Electrical
Synchronized cardioversionVT: 120–150 J first, then step upUnstable patients. Also the UK first choice for stable monomorphic VT with structural or unknown heart diseaseSedate or anesthetize if conscious, and expect sedation to worsen hemodynamics.1
Regular, monomorphic: drugs
Procainamide10–15 mg/kg IV over 20 min (max 1 g)Stable VT; first-line drug in the UK algorithmLabel: no faster than 50 mg/min; stop for hypotension, persistent conduction problems, or QRS widening of 50%. Contraindicated in torsades and lupus.1,8
Amiodarone300 mg IV over 10–60 min, then 900 mg over 24 hStable VT if procainamide is unavailable or contraindicatedUS label load: 150 mg over 10 min, then 1 mg/min for 6 h, then 0.5 mg/min. Hypotension in 16% in label trials.1,13
Adenosine6 mg rapid IV, then 12 mg, then 18 mgRegular, monomorphic rhythm that may be SVT, with no pre-excitationUS label: 6 mg, then 12 mg, repeated once. Avoid in bronchospasm.1,14
Polymorphic VT with a long QT (torsades)
Magnesium8 mmol IV over 10 minTorsadesAvoid amiodarone. Consider isoprenaline or pacing to raise the heart rate.1
Avoid
Verapamil or diltiazemDo not giveUndifferentiated wide-complex tachycardiaHemodynamic deterioration in every misdiagnosed VT treated with verapamil.5
LidocaineNot first-line—Terminated 3 of 14 VTs vs 12 of 15 with procainamide.15

Unreviewed doses. Verify against the current label and your institution's protocol before giving anything.

Sources disagree

For a stable patient in monomorphic VT, the UK guideline recommends electrical cardioversion when there is structural heart disease or the heart's state is unknown, and keeps drugs for patients in whom sedation is too risky.1,2 The 2025 American Heart Association guideline, as summarized, suggests vagal maneuvers and drug therapy for stable wide-complex tachycardia.9,10 Either way, shock if the patient becomes unstable.1

Procainamide or amiodarone?

  • PROCAMIO (n = 62 analyzed, tolerated wide-complex tachycardia, probably VT): procainamide 10 mg/kg over 20 min vs amiodarone 5 mg/kg over 20 min. Major cardiac adverse events within 40 min: 9% vs 41%. Termination within 40 min: 67% vs 38%. In structural heart disease, adverse events were 11% vs 43%.6
  • Amiodarone terminates VT poorly. In an ED series it stopped 8 of 28 VTs (29%) within 20 minutes.16 In another, it stopped 15% within 20 minutes and 29% within an hour; 17% needed emergency cardioversion for hemodynamic deterioration.17
  • A systematic review (5 small studies) found procainamide, ajmaline and sotalol all better than lidocaine. Amiodarone was not more effective than procainamide.18
  • Lidocaine: in a randomized trial, procainamide stopped 12 of 15 VTs and lidocaine 3 of 14.15

Adenosine

  • In 197 ED patients with a regular wide-complex tachycardia, 90% of SVTs and 2% of VTs responded to adenosine. A response raised the odds of SVT 36-fold. No patient needed emergency treatment for an adenosine side effect.7
  • Use it only for a regular, monomorphic rhythm. The UK algorithm gives it only when there is no pre-excitation, and says to treat as VT if it fails.1
  • Adenosine does not convert VT. Rare ventricular fibrillation has been reported, mostly with digoxin.14

Torsades

In 12 patients with torsades, a 2 g magnesium sulfate bolus abolished it in 9, and a second bolus worked in the other 3. Magnesium did not help polymorphic VT with a normal QT. Most episodes were caused by antiarrhythmic drugs, and 8 patients had potassium below 3.5 mEq/L.19

After the rhythm is controlled

  • Persistent arrhythmias often mean structural heart disease or unresolved problems such as myocardial ischemia. Look for both.1
  • Get expert help if the arrhythmia or life-threatening features persist.1
  • Watch the blood pressure after amiodarone. Hypotension is its most common adverse reaction, usually in the first hours and related to the infusion rate. Treat it first by slowing the infusion.13
  • Watch for bradycardia and AV block after amiodarone; some patients need pacing.13

Pitfalls

  • Calling it SVT without looking for AV dissociation. It was visible on 73% of the ECGs of misread VT.5
  • Giving verapamil or diltiazem before VT is excluded.5
  • Giving adenosine for an irregular wide-complex rhythm, or with pre-excitation.1
  • Trusting one ECG algorithm to rule VT out. Specificity is only moderate.11,12
  • Treating torsades with amiodarone or procainamide. Use magnesium.1,8
  • Missing a metabolic cause, such as hyperkalemia or sodium channel blocker toxicity, that widens the QRS of an SVT.4

How strong is the evidence?

Most of the evidence is small and old. Only one randomized trial compares the two main drugs, and it analyzed 62 patients.6 The systematic review of drug therapy found quality problems in all five studies.18 Recommendations on cardioversion versus drugs for stable VT differ between the UK and US guidelines.1,9 Neither the full ERC nor the full AHA guideline text could be read for this page.2,9

On-shift teaching

Questions to ask a learner at the bedside. Tap a question to see the answer. Every answer uses facts cited above.

Q1Why is verapamil dangerous in a wide-complex tachycardia?
Because VT is easily mistaken for SVT. In one series, 15 of 38 VTs (39%) were called SVT. Verapamil was given in 13 of them, and all 13 deteriorated.5
Q2Which parts of the history make VT likely?
Prior myocardial infarction, heart failure, or recent angina each had a positive predictive value for VT over 95%. Age over 35 had 92% sensitivity. No history feature strongly predicted SVT.3
Q3Can an ECG algorithm rule VT out?
No. Pooled across 14 studies, the algorithms had 89% sensitivity and 71% specificity.11 In a head-to-head test, all five methods had only moderate accuracy.12 Treat as VT when in doubt.4
Q4Is adenosine safe in a regular wide-complex tachycardia?
In 197 ED patients it caused no adverse event needing emergency treatment, and 90% of SVTs but only 2% of VTs responded.7 Use it only for a regular, monomorphic rhythm without pre-excitation.1
Q5Procainamide or amiodarone for stable VT?
Procainamide. In PROCAMIO it caused fewer major cardiac adverse events (9% vs 41%) and terminated more tachycardias within 40 minutes (67% vs 38%).6 The UK algorithm also lists it first.1
Q6Polymorphic VT with a long QT. What do you give, and what do you avoid?
Magnesium, 8 mmol IV over 10 minutes, and consider isoprenaline or pacing to raise the rate. Avoid amiodarone.1 In 12 patients, 2 g magnesium sulfate abolished torsades in 9 with one bolus and in the rest with a second.19

References

Evidence base

What this page is built on

19 sources, cited 96 times. Dots are sources, filled by how far each was read; stronger color means a larger share of the citations. Tap a tier to see its sources.

Read in full · 6Abstract read · 11Record only · 2Link checked · 0

Checked by the writer, not a physician. The dots show how each source was read, not that anyone has confirmed the claims.

How this page was made
  • Written from scratch. No source text was copied; facts are restated and cited.
  • Anchored on the Resuscitation Council UK 2025 adult advanced life support guideline, which adapts the ERC 2025 guideline, and its tachyarrhythmia algorithm (updated March 2026); both were read in full. The ERC 2025 and AHA 2025 guideline full texts, and the 2017 AHA/ACC/HRS and 2022 ESC ventricular arrhythmia guidelines, could not be accessed. AHA recommendations are given only as summarized by EM Ottawa, and are cited to both.
  • Each PubMed citation was resolved through NCBI E-utilities and checked against its abstract. Doses come from the UK guideline and FDA labels on DailyMed; where they differ, both are shown.
  • Figure 1 was drawn for this page from cited sources. Figure 2 is an openly licensed image from Wikimedia Commons, credited under it, and keeps its own license.
  • Adults only. Wide-complex tachycardia in children was not reviewed for this page.
  • Not for clinical use.
Not for clinical use

AI-generated draft. Not reviewed by a physician. This page is for education only and may contain errors, including in doses. Do not use it to diagnose, treat or make decisions about any patient. Rely on your own clinical judgment, your institution's protocols and current drug labeling. Reading this page does not create a physician-patient relationship. Full terms