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WCT

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Ibtisam Al-Hoqani

Ibtisam Al-Hoqani

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  • 1. Ibtisam Al Hoqani EM – R2 31/8/2010 Approach to Wide Complex Tachycardia
  • 2. Outline :
    • Basic ECG
    • What is WCT
    • Mechanisms of WCT
    • Diagnostic criteria
    • Management
    • Take home message
  • 3. The Normal Conduction System
  • 4. what is this rhythm ?
  • 5. Normal Intervals
    • PR
      • 0.20 sec (less than one large box)
    • QRS
      • 0.08 – 0.10 sec (1-2 small boxes)
    • QT
      • 450 ms in men, 460 ms in women
      • Based on sex / heart rate
      • Half the R-R interval with normal HR
  • 6. Differential Diagnosis of Tachycardia Tachycardia Narrow Complex Wide Complex Regular ST SVT Atrial flutter ST with aberrancy VT Irregular A-fib A-flutter with variable conduction MAT A-fib with aberrancy A-fib with WPW PVT
  • 7. What is this rhythm?
  • 8. What is WCT?
    • It is refers to dysrhythmias with rate greater than 100 beats/min associated with QRS complex duration of more than 0.12 sec
    • It is divided to:
    • =Regular
    • =Irregular
  • 9.  
  • 10. Causes of WCT :
      • Irregular WCT:
      • Afib with BBB or IVCD (pre-existent or rate related)
      • Afib with anterograde conduction over accessory pathway in WPW
      • Polymorphic VT ex: Torsades de pointes or due to Digitalis intoxication
      • Other causes of an irregular rhythm ( A flutter with variable conduction, MAT etc) with BBB, WPW, IVCD
  • 11.  
  • 12. Causes of WCT:
    • Regular rhythm:
    • Ventricular driven rhythm:
      • VT : worst case scenario
    • Supraventricular rhythm with aberrant conduction:
      • SVT with BBB
      • SVT with accessory pathway Ex: WPW
  • 13. How to distinguish SVT from VT
    • Focus History
    • Physical examination
    • ECG tracing
    • Using specific Criteria :
    • Wellens criteria
    • Brugada criteria
  • 14. Preceding P waves with QRS QRS <0.14 Normal axis Slow or terminate with vagal maneuvers Fusion beats AV dissociation QRS >0.14 Extreme LAD No response to vagal maneuvers ECG Absence of variability Cannon A wave Variation in arterial pulse Variation in S1 Physical examination Mitral valve prolapse (WPW) Previous Hx of SVT Age>50 Hx of MI, CHD, CABG, ASHD Mitral valve prolapse Previous Hx of VT History SVT with aberrancy VT
  • 15.  
  • 16.  
  • 17. Management of WCT Any new onset symptomatic WCT is VT until proven otherwise
  • 18. Management of WCT
    • If the patient is hemodynamically unstable, the first - choice therapy for ventricular tachycardia (VT) is synchronized direct-current (DC) cardioversion with 50 – 100 J
    • If the patient is suffering from monomorphic VT and has a preserved heart function, the first-line treatment is lidocaine . Alternatives include either amiodarone or procainamide .
  • 19.
    • If the patient has polymorphic VT with a normal baseline QT interval, AHA guidelines state that the first steps are to treat ischemia and correct any electrolyte imbalance .
    • If cardiac function is impaired, use amiodarone or lidocaine, followed by synchronized DC cardioversion
  • 20.
    • If the patient has polymorphic VT with a prolonged baseline QT interval, ACLS guidelines state that any electrolyte imbalance should be corrected . Following this, any one of these treatments can be administered : magnesium sulfate , overdrive pacing, or lidocaine
  • 21.
    • Long - term treatment of sustained ventricular arrhythmias includes placement of an implantable cardioverter -defibrillator (ICD) and possible adjunctive therapy with amiodarone or sotalol in certain subsets of patients. Patients should be under the care of a cardiologist or electrophysiologist
  • 22.  
  • 23. Take home message
    • Any new onset symptomatic WCT is VT until proven otherwise
    • About 80% of all WCT are ventricular tachycardia
    • In patients with known structural heart disease almost all WCT are ventricular tachycardia

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