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October 21, 2025 Circulation. 2025;152(suppl 2):S538–S577. DOI: 10.1161/CIR.0000000000001376 S562 Wigginton et al Advanced Life Support: 2025 AHA Guidelines for CPR and ECC WIDE-COMPLEX TACHYCARDIA Recommendations for the Management of Adult Patients With Wide- Complex Tachycardia COR LOE Recommendations 1 B-NR 1. Synchronized cardioversion is recommended for acute treatment of adult patients with hemodynamically unstable wide-complex tachycardia. 1 B-NR 2. Synchronized cardioversion is recommended for acute treatment of adult patients with hemodynamically stable wide-complex tachycardia when vagal maneuvers and pharmacological therapy is ineffective or contraindicated. 2b B-R 3. Administration of IV amiodarone, procainamide, or sotalol may be considered for the treatment of adults with wide-complex tachycardia. 2b B-NR 4. In hemodynamically stable adult patients with regular monomorphic wide-complex tachycardia, IV adenosine may be considered for treatment or aiding rhythm diagnosis when the cause of the rhythm cannot be determined. 3: Harm B-NR 5. Verapamil and diltiazem should not be administered for adult patients with wide-complex tachycardia. 3: Harm C-LD 6. Adenosine should not be administered for adult patients with hemodynamically unstable, irregularly irregular, or polymorphic wide-complex tachycardia. Synopsis Wide-complex tachycardia (WCT) is generally defined as a rhythm greater than 150/min with a QRS duration of 0.12 second or more.1,2 There are 4 means of achieving a wide QRS complex: (1) conduction of ventricular origin, (2) left or right bundle branch block, (3) conduction through a bypass tract, and (4) ventricular pacing. Rarely, hyperkalemia or sodium channel blockade can present with a WCT. Thus, WCTs can be ventricular (VT or VF), or supraventricular tachycardias resulting from mechanisms 2, 3, or 4. WCT can have a monomorphic or nonmonomorphic (ie, polymorphic) QRS. Polymorphic QRS complexes are typical of torsades de pointes, VF, or AF with a bypass tract. Most other rhythms are monomorphic. Patients with WCT can be hemodynamically stable or unstable. Hemodynamically stable patients with WCT allow the professional time to obtain a 12-lead electrocardiogram, place an IV, and administer IV drugs, while patients who are unstable require prompt cardioversion (Figure 6). Recommendation-Specific Supportive Text 1 In hemodynamically unstable patients with WCT it is critical to promptly restore sinus rhythm. If the patient is unstable as a result of the WCT (eg, systolic blood pressure <80 mm Hg or altered mentation) immediate synchronized cardioversion is warranted.3 2 In stable patients with WCT, vagal maneuvers or adenosine may be attempted; however, if the patient remains in WCT following these therapies, synchronized cardioversion is recommended. If time and clinical stability permits, administration of procedural sedation may be appropriate.3 3. Amiodarone has a relatively slow onset of action, and some solutes may cause hypotension. IV procainamide can also cause hypotension and must be infused no faster than 50 mg/min. IV sotalol is a newer agent without these concerns for hypotension. Direct comparisons of efficacy are generally between lidocaine and these three antiarrhythmic medications. Lidocaine’s kinetic properties are less effective for VT at hemodynamically tolerated rates than amiodarone, procainamide, or sotalol,4 and it is unclear if lidocaine is more efficacious than placebo. Conclusions based on limited available evidence from small heterogeneous human studies for the treatment of stable, monomorphic VT, procainamide and sotalol each appear to have similar efficacy; amiodarone was not more effective than procainamide.5–9 Avoiding coadministration of these drugs is important because their combined effects may be arrhythmogenic. When any of these drugs are administered, the immediate availability of a defibrillator is encouraged because each drug may convert a WCT to a more rapid, malignant (ie, hemodynamically unstable) form, depending upon its underlying cause. 4. Adenosine blocks the atrioventricular (AV) node and decreases automaticity. Thus, WCTs in which the AV node is part of the circuit will be terminated by an effective dose of adenosine as described in therapies for narrow-complex tachycardia (NCT). Adequate adenosine administration may momentarily block the AV node, allowing the underlying rhythm to be correctly assessed. Therefore, adenosine can be diagnostic and therapeutic in a stable, regular, monomorphic WCT.10,11 5 Verapamil is a calcium channel blocker that slows AV node conduction, shortens the refractory period of accessory pathways, and acts both as a negative inotrope and vasodilator. The vasodilatory effects are relatively profound, and thus, hypotension is common with administration. Verapamil will not terminate a WCT of ventricular origin and may cause profound hypotension leading to shock and cardiac arrest.12,13 6 Adenosine will not terminate a WCT of ventricular origin, may cause profound hypotension leading to shock, or precipitate VF and cardiac arrest.14,15 REFERENCES 1 Page RL, Joglar JA, Caldwell MA, Calkins H, Conti JB, Deal BJ, Estes NA 3rd, Field ME, Goldberger ZD, Hammill SC, et al; Evidence Review Committee Chair‡. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2016;133:e506–e574. doi: 10.1161/CIR.0000000000000311 2. Al-Khatib SM, Stevenson WG, Ackerman MJ, Bryant WJ, Callans DJ, Curtis AB, Deal BJ, Dickfeld T, Field ME, Fonarow GC, et al. 2017 AHA/ACC/ Downloaded from http://ahajournals.org by on October 7, 2026