Cardiology Report 1/23/18 – WCT

Thank you to Ashley for presenting a case of an elderly man who presented with sub-acute palpitations and SOB, found to have an irregular wide complex tachycardia, ultimately found to have an accessory pathway!

Key Pearls:

  • Once a patient has afib, they effectively always have afib – even if after an ablation they return to sinus rhythm. Make decisions for anticoagulation based on the patient’s Chads-Vasc2.
  • The symptom most predictive of current left-sided heart failure, is paroxysmal nocturnal dyspnea with a LR of 2.6 (see the chart from the JAMA Rational Clinical Exam below that shows LR of other historical elements, symptoms, and physical exam findings).
  • Cannon a waves, a pulsation that happens when the atria contract against a closed tricuspid valve, can help identify A-V dissociation even before you see the ECG.
  • With an irregular wide complex tachycardia, the medication of choice is procainamide. This stems from a need to avoid AV nodal blockade (adenosine, BB, CCB) as you cannot rule out the presence of atrial fibrillation with an accessory pathway. If the patient has an accessory pathway and you block the AV node, you could shunt the rhythm through the accessory pathway which may have a very short refractory period and result in extremely fast rates and degeneration into an unstable rhythm.

Jama Rational Clinical Examination. Does this Dyspneic Patient in the ED Have CHF?


Approach to a Regular Wide Complex Tachycardia

There’s a relatively short differential diagnosis for Wide Complex Tachycardia. The most important entity to rule out is ventricular tachycardia.

Step 1: Hemodynamic Instability? If present à manage as if Ventricular Tachycardia and perform synchronized cardioversion. If HD stable, you have time to think (and to breath!) – go to Step 2.

Step 2: Turn to your DDx for WCT

  • VT
  • SVT with aberrancy
  • antidromic AVRT
  • Pacemaker mediated tachycardia
  • med or electrolyte-mediated widening of the QRS + tachycardia (such as TCA overdose, hyperkalemia)

Could this be VT?

  • A-V dissociation (p’s and QRS’s not marching together)
  • Fusion beats or Capture beats (further evidence of A-V dissociation)
  • Concordance in the precordial leads (all are positive or all are negative)
  • The wider the QRS, the more likely to be VT
  • NW axis (+ in aVR), more likely to be VT
  • Morphology criteria

Check out this approach to VT from a prior set of Pearls from Rabih:



WCT Evernote:


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