Wide-Complex Tachycardia

Wide-complex tachycardia means a QRS of 120 ms or more at a rate above 100/min. This page uses 100/min as its working line. The 2025 AHA Part 9 definition is generally a rate above 150/min with a QRS of 0.12 s or more. Its ACLS algorithm applies at 150/min or more. There are two ways the QRS ends up wide. In ventricular tachycardia (VT), the impulse starts in the ventricle and crawls from muscle cell to muscle cell. That is slower than conduction through the His–Purkinje system. In supraventricular tachycardia (SVT) with aberrancy, the impulse starts above the ventricles. It gets there by an abnormal route, such as through an existing bundle branch block or a rate-related one. A third mechanism is pre-excitation. An accessory pathway lets atrial impulses reach the ventricle without the AV node's delay. So the QRS width changes from beat to beat.

VT usually comes from scarred or ischemic muscle. That is why it is common after a myocardial infarction and in cardiomyopathy. The ventricles can beat without waiting for the atria. So atrioventricular (AV) dissociation is the most specific clue that the QRS starts in the ventricle.

Start with the widest lead, because its QRS width is the first thing that sorts these rhythms. Then check regularity and the AV relationship. Decide stability before any drug goes in.

1. Select the widest lead, usually II, V1 or V5. Use V1 and aVR for the morphology steps.
2. Measure the QRS from onset to end in ms (one small box is 40 ms); 110–119 ms is borderline.
3. Check the R-R intervals across at least three beats to decide whether the rhythm is regular.
4. Look for P waves before each QRS, and for capture and fusion beats that show AV dissociation.
5. Assess stability before choosing an algorithm; an unstable patient is treated first.

Three or more consecutive ventricular beats above 100/min is VT. It counts as sustained if it lasts 30 seconds or longer, or if it needs intervention. Monomorphic VT has one QRS shape. Polymorphic VT and torsades de pointes change shape and axis. They get their own lesson on the Ventricular Rhythms page.

ECG Criteria

• QRS: 120 ms or more, usually bizarre compared with the patient's sinus beats
• AV dissociation: P waves march through at their own rate and do not match the QRS
• Capture and fusion beats: A narrow QRS inside the wide run (capture) or a QRS that merges two shapes (fusion) favors VT
• Precordial pattern: No RS complex in any precordial lead (V1–V6) is highly specific for VT in the Brugada algorithm
• Concordance: All precordial QRS complexes (V1–V6) are positive, or all are negative; this favors VT
• Extreme axis: A northwest axis (between −90° and ±180°) favors VT
• Very wide QRS: Over 160 ms favors VT, especially with a bundle branch pattern

Causes

• Ischemia or prior myocardial infarction (scar-related re-entry), including acute ischemia
• Cardiomyopathy, structural heart disease and heart failure
• Electrolyte disturbance: hypokalemia, hypomagnesemia and hyperkalemia
• Drugs and toxins: class I antiarrhythmics, tricyclic antidepressants and other sodium-channel blockers, and digoxin toxicity

Clinical Significance

• Sustained VT with a pulse can deteriorate to ventricular fibrillation. It can also cause hypotension, heart failure or shock
• Heart disease changes the picture. Non-sustained VT in that patient needs evaluation for ischemia, scar and cardiomyopathy
• When the rhythm is uncertain, treat it as VT. Treating SVT as VT usually costs less than missing VT

In SVT with aberrancy, a supraventricular impulse takes an abnormal path to the ventricles. The QRS widens only for as long as the aberration lasts. Rate-related aberrancy (Ashman phenomenon) shows up at fast rates or after a long pause. It is a bundle branch pattern that disappears at slower rates. How SVT itself works is taught on the Atrial Rhythms page.

ECG Criteria

• P waves: An atrial activity pattern that is related to each QRS, or a regular 1:1 atrial rhythm you can follow through the wide complexes
• QRS morphology: Usually resembles a bundle branch block, often without the bizarre shape of VT
• Comparison: An old ECG, or a slower strip with the same QRS, shows whether the width is rate-related

Causes

• AV nodal re-entrant tachycardia (AVNRT) or AV re-entrant tachycardia (AVRT) with a pre-existing bundle branch block
• Atrial fibrillation or flutter with a rapid ventricular response and a pre-existing bundle branch block
• Rate-related aberrancy after a long pause, or a pre-existing bundle branch block that becomes wider at fast rates

Clinical Significance

• A known bundle branch block is the classic trap. That wide QRS can be aberrant SVT. It can also be VT. Compare with an old ECG
• Adenosine can slow or stop the rhythm and show the atrial activity. If the rhythm does not change, manage it as VT. Stopping the rhythm does not rule out adenosine-sensitive VT. Review the 12-lead after any change

Pre-excited atrial fibrillation means atrial impulses reach the ventricles two ways: over an accessory pathway and through the AV node. The pathway does not slow conduction the way the node does. So many impulses can arrive at the ventricle very quickly. Each impulse fuses differently with the node pathway, so the QRS width and shape change from beat to beat. AF itself is taught on the Atrial Rhythms page. The delta wave lives on the PR Interval page.

ECG Criteria

• Rhythm: Irregular, with R-R intervals that vary
• QRS: Wide, with a width and shape that vary from beat to beat; the rate is often very fast
• Baseline clue: A short PR interval with a delta wave on a sinus ECG suggests an accessory pathway (see PR Interval)

Causes

• Wolff-Parkinson-White syndrome or another accessory pathway
• Any AF trigger in a patient with a known accessory pathway

Clinical Significance

• Very fast conduction over an accessory pathway can degenerate into ventricular fibrillation. That is why AV nodal blockers are dangerous
• Catheter ablation of the accessory pathway is the definitive treatment (2023 ACC/AHA/ACCP/HRS AF guideline, Class 1)

Rhythm by Type

Two published algorithms split VT from SVT with aberrancy by QRS shape. Both are sensitive. Neither is specific. When the diagnosis is uncertain, a VT call is the safer default.

Brugada Algorithm (1991)

1. Step 1: No RS complex in any precordial lead (V1–V6): VT
2. Step 2: RS interval longer than 100 ms in any precordial lead: VT
3. Step 3: AV dissociation: VT
4. Step 4: Morphology criteria in V1 and V6: VT if met; if none apply, SVT with aberrancy. Use the exact criteria in the 1991 paper

Vereckei aVR Algorithm (2008)

1. Step 1: Initial R wave in lead aVR: VT
2. Step 2: Initial r or q wave wider than 40 ms: VT
3. Step 3: Notch on the initial downstroke of a predominantly negative QRS in aVR: VT
4. Step 4: Ventricular activation-velocity ratio (initial versus terminal 40 ms) above 1 suggests SVT; 1 or less suggests VT

Accuracy

A 2023 meta-analysis of 14 studies (3,966 patients) found high sensitivity at 88.89% overall. Specificity was moderate, at 70.55%. RWPT-II had the highest pooled specificity (88.30%) and the lowest sensitivity (78.15%). The authors suggest the Brugada or Vereckei aVR algorithm, combined with RWPT-II, could be considered. These are pooled secondary-analysis figures. They are not guidance for a single patient.

VT Versus SVT With Aberrancy Versus Pre-Excited AF

Mimics

• Hyperkalemia and sodium-channel blockade: They produce a wide QRS from a different cause. Treat the cause (see QRS Complex and T Wave). An antiarrhythmic is not the answer
• Torsades de pointes: polymorphic VT with a long QT interval; see QT Interval
• Paced rhythm: a wide QRS with a left bundle pattern is what pacing produces. Look for pacing spikes and the device history

Artifact & Lead Misplacement

• Tremor, shivering or transport vibration: It can mimic VT or ventricular fibrillation. Confirm with a second lead or a pulse check
• Limb lead reversal: It changes lead I and aVR. That matters for the Vereckei steps
• Precordial misplacement: Electrodes placed high on V1 or V2 change the precordial pattern. The Brugada steps read that pattern

The doses below come from the 2025 AHA ACLS tachyarrhythmia algorithm. They line up with the linked medication and intervention pages.

Hyperkalemia and sodium-channel toxicity: Go after the cause. For tricyclic-type toxicity with QRS widening, the first-line antidote is sodium bicarbonate: 50–150 mEq IV bolus for adult TCA or tetracyclic cardiotoxicity (2025 AHA Part 10, COR 1, B-NR). For children, 1–3 mEq/kg, and never above the adult dose (see Sodium Bicarbonate). In hyperkalemia, calcium steadies the myocardium while potassium is shifted (see Calcium Chloride and Insulin).

The dosing here comes from the 2025 AHA ACLS tachyarrhythmia algorithm and the linked pages.

Pediatrics

• Infant and child SVT: Infant SVT is usually above 220 bpm. Child SVT is usually above 180 bpm. A wide complex in a child can be SVT with aberrancy. If perfusion is poor or the rhythm is uncertain, treat it as VT with synchronized cardioversion. PALS calls a QRS over 0.09 s wide
• Pediatric VT: Uncommon. It is usually linked to congenital heart disease, cardiomyopathy or a channelopathy. An expert should review the rhythm
• Cardiopulmonary compromise: Unstable: synchronized cardioversion (0.5–1 J/kg, then 2 J/kg if the first shock fails). Stable with a regular, monomorphic QRS: adenosine can be useful with expert consultation (2025 AHA Part 8, WCT rec 2, COR 2a). Watch a running rhythm strip, with cardioversion kept ready. Never for an irregular QRS
• Congenital heart disease: After surgical repair, wide-complex rhythms are common. Pull the surgical history. Check for epicardial pacing wires and look at the atrial rhythm
• Dosing: Weight-based doses follow the Weight-Based Dosing

Other Populations

• Pregnancy: Unstable: shock promptly. In cardiac arrest, fetal monitoring should not delay defibrillation (2025 AHA Part 10, pregnant patients, supportive text). Stable: correct magnesium and potassium. If the patient progresses to cardiac arrest with the fundal height at or above the umbilicus, give manual left lateral uterine displacement with compressions (2025 AHA Part 10, pregnant patients rec 4, COR 1, LOE C-LD). Remove the fetal monitors. They should not be used during arrest (rec 9, No Benefit). Amiodarone can cause fetal thyroid and neurodevelopmental effects (label). Weigh that against VT treatment with expert input
• Heart transplant recipients: The denervated heart responds unusually to adenosine, and the effects may be profound. The 2025 AHA Part 9 (NCT section) notes that 1 mg IV may be enough to terminate the rhythm. Start low and titrate per the Adenosine page
• Older adults and structural heart disease: Ischemia and scar are common causes. A new wide QRS needs a 12-lead and serial ECGs
• Pacemaker or ICD: Paced beats and device therapy can produce wide complexes. Ask for device interrogation. Review the shock history before you give an antiarrhythmic

1. Decide whether the patient is stable or unstable before reading the strip in detail.
2. Measure the QRS in the widest lead and confirm it is 120 ms or more.
3. Check regularity. A wide and irregular rhythm is pre-excited AF until proven otherwise.
4. Look for AV dissociation, capture beats and fusion beats.
5. For a regular rhythm, apply the Brugada precordial steps and the Vereckei aVR steps.
6. Treat by the stability row in the bedside table. Never give an AV nodal blocker to an irregular rhythm.
7. Reassess after each drug and cardioversion: recheck the 12-lead, the pulse and the rhythm.

Common Pitfalls

• Calling a wide complex SVT because the patient has a known bundle branch block, without an old ECG for comparison
• Giving adenosine to an irregular wide-complex rhythm
• Calling a paced rhythm VT or SVT without checking the pacing history
• Treating electrical activity on the monitor as a perfusing rhythm when there is no pulse
• Using QRS width alone; the algorithms need the AV relationship and the precordial pattern
• Stacking antiarrhythmics such as amiodarone and procainamide without expert input