Lesson 8: Wide Complex Tachycardia

Summary of Learning points

• Normal QRS duration = 60-100 msec

  • Wide QRS = QRS duration > 120 msec (3 little boxes)

• Differential diagnosis for wide QRS complex tachycardia:

  • SVT with permanent BBB (fixed conduction defect  block is present at any heart rate)

  • SVT with rate-dependent BBB (prolonged bundle branch refractory period  no block below a critical heart rate, though block manifests at higher HR)

  • SVT with pre-excitation (accessory pathway)

    • Accessory pathway allows atrial impulse to bypass AV node

    • Example: WPW (Wolff-Parkinson-White)  accessory pathway causing early depolarization of ventricular tissue close to the insertion of the accessory pathway, which shows up on ECG as a delta wave

    • Allows for the existence of AVRT, a re-entrant circuit including both the AV node and the accessory pathway

      • Orthodromic AVRT: narrow QRS complex (impulse travels to the ventricles normally through the AV node, but returns to the atria abnormally through the accessory pathway)

      • Antidromic AVRT: wide QRS complex (impulse travels to the ventricles abnormally through the accessory pathway, causing initial slow cell-to-cell depolarization leading to wide QRS complex, but returns to the atria via retrograde conduction through the AV node)

  • VT

    • Definition: 3 consecutive ventricular depolarizations at a rate > 100 bpm

      • Ventricular rhythm with rate < 100 bpm = usually AIVR (accelerated idioventricular rhythm)

    • Can be monomorphic (QRS complexes all the same amplitude) or polymorphic (multiple QRS amplitudes)

    • Caused by re-entry circuits around areas of prior myocardial scar or by triggered activity (eg the “R-on-T” phenomenon that induces torsades de pointes, a specific subcategory of polymorphic VT)

    • Common misconceptions:

      • VT is NOT always fast! Can have rates <150 or even <130 if on antiarrhythmics

      • VT is NOT always hemodynamically unstable! People can be minimally symptomatic in VT, especially at lower heart rates

      • Other commonly discussed ECG tricks (precordial concordance, “northwest” or extreme right axis deviation) are useful but not 100% specific even when present

  • Toxic or metabolic abnormality

    • Digoxin toxicity, TCA overdose, sodium channel blocker overdose, electrolyte abnormalities

• What to do when you see a wide complex rhythm:

  • Is the patient hemodynamically unstable?

    • If so, it doesn’t matter what the rhythm is – cardiovert them (AFTER YOU SEDATE THEM) and figure out the rhythm later

  • Patient factors:

    • Older, known structural heart dz, prior infarct ischemia  more likely VT

    • Younger, prior BBB with identical morphology to current ECG, evidence of WPW  more likely SVT

    • If unsure, assume VT until proven otherwise

  • Look in more detail at the ECG!

    • AV dissociation: P waves and QRS complexes at different frequencies

      • Can manifest with fusion beats (supraventricular + ventricular beat occurring at the same time  weird looking “hybrid” complex) or capture beats (a supraventricular impulse occurs just at the right time to “capture” the ventricles), but these usually only occur at lower heart rates

    • QRS duration: if QRS duration > 160 ms, more likely VT

      • Remember to measure the QRS from the earliest start of the QRS complex in any lead to the latest termination of the QRS complex in any lead (even if it’s a different lead!)

    • Other factors that favor VT:

      
      

      

      
      

Practice ECG

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