wide complex tachycardia

Introduction

Wide complex tachycardias may occur as a result of initial supraventricular or ventricular depolarizations. Identification of the origin of the initial depolarization is important in selection of the appropriate management of the patient.

Etiology

• ventricular tachycardia (most common)
• supraventricular tachycardias (SVT):
  • SVTs associated with bundle-branch block
  • Wolf-Parkinson-White (WPW)

Diagnostic procedures

• electrocardiogram, establish the rhythm
• electrophysiologic testing after restoration of sinus rhythm
• saO2

Management

• treat as ventricular tachycardia until proven otherwise
  • adenosine may be given for stable wide complex tachycardia to determine with it is supraventricular tachycardia (SVT) vs ventricular tachycardia (SVT will respond to adenosine)
• unstable patients
  • immediate synchronized cardioversion
• stable patients with suspected supraventricular tachycardia
  • adenosine 6 mg IV, followed by 12 mg IV if no effect
  • carotid sinus massage
• pharmaceutical agents
  • beta-blocker for atrial fibrillation with bundle branch block
  • amiodarone 150 mg IV over 10 min for ventricular tachycardia
    • repeat as needed to maximum dose of 2.2 g/24 hours
  • chemical cardioversion
    • procainamide is the agent of choice for chemical cardioversion of ventricular tachycardia except in the setting of acute MI or digoxin toxicity; in these cases, lidocaine remains the agent of choice; procainamide may also terminate supraventricular arrhythmias
  • consider sedative (benzodiazpeine, barbiturate) with or without analgesic (opiate)
• at bedside:
  • suction device
  • IV line
  • setup for endotracheal intubation
• inpatient monitoring following restoration of sinus rhythm

More general terms

• tachyarrhythmia (tachycardia)

More specific terms

• accelerated idioventricular rhythm (AIVR)
• ventricular tachycardia (VT)

Additional terms

• Wolff-Parkinson-White (WPW) syndrome