Wide Complex Tachycardia

  • Based on site of origin of Tachycardia, can be either, SVT or VT
  • But in clinical practice, duration of QRS is the first guide in identifying the nature of tachycardia 
    • Narrow Complex 
    • Wide Complex 

Wide complex SVT
  • 3 Causes 
    • Pre-existing BBB
    • SVT with Right or Left bundle aberrancy
    • Atrial Fibrillation with pre excitation
      • Antidromic Tachycardia
      • Do not give adenosine. 
      • Recognising this is perhaps the most important.  

Understanding Tachycardia
  • Even before you look at any EKG, you need to understand the following to make sense of any EKG 
    • First: Be able to define narrow complex and wide complex tachycardia 
    • Then, understand the cardiac conduction pathway, and review the sequences of normal ventricular activation. Knowing this - 
    • Understand how does narrow complex and wide complex QRS occur. Knowing this - 
    • Locate the possible site of origin of cardiac conduction, and its propagation into the ventricle in the narrow complex tachycardia and in wide complex tachycardia 
      • Narrow and Wide Complex
      • PR segment present or absent (as in pre excitation)
      • Jump wave if seen 
    • Know the pathophysiology of tachycardia 
  • After this you are ready to look at an EKG 
    • In order to avoid misdiagnosis, few catch points, or not to miss points while reviewing EKG are 
      • Always use caliper or tool in computer. 
      • Always have a same sequence of reviewing EKG. 
      • And, review EKG in its entirety. 
      • Understand, normal looking p wave can occur in AT if the origin of atrial tachycardia is near SA Node 
      • In reviewing Narrow Complex tachycardia, 
        • Look for PR and RP relationship 
          • Short PR Tachycardias and Long PR tachycardias are different 
            • Short RP Tachycardia 
            • Long RP Tachycardia
              • Atrial tachycardia
              • Atypical AVNRT
              • ORtw with a slow decremental pathway (PJRT)
        • Understand AT typically does not exceed 200 atrial bpm
        • Look for Isoelectric line to differentiate AT from A flutter . 
          • Atrial flutter has no isolectric line that is representation of atrial depolarization
            • 2 exception
              • If prior history of cardiac surgery or ablation is present, it is atrial flutter even if isoelectric lines are present 
        • Look for uniformity of morphology. 
          • Flutter wave in atrial flutter is of same morphology. If different morphology is present, then it may actually be Atrial Fibrillation
      • 10-20 % of Atrial Tachycardia can respond to Adenosine. Just a response to Adenosine does not mean it is AV node involved tachycardia.

  • Definition:
    • Rate > 100 bpm
    • QRS > 120 msec
  • Ventricular activation is slow due to 
    • Site of origin is either at or below his bundle, or in perkinje fibers, or ventricular myocardium OR
    • Site of origin is SVT but there is a preexisting conduction abnormalities in the his-purkinje system, like BBB, or rate related aberrancy
    • Site of origin is SVT but there is a ventricular pre excitation i.e part of ventricle activates through alternate pathway while simultaneously part of the ventricle is activating through his-purkinjee system
      • How much ventricle activates from alternate pathway or abberent pathway depends on how far is the abberent pathway from AV Node. Closer it is, more symptomatic it will be
  • Etiology : 4 categories 
    • V Tach
    • SVT with abnormal ventricular activation
      • Aberrant conduction via normal conduction pathway (in BB, or distal purkinji system)
        • BBB, IVCD (intraventricular conduction delay), rate-related aberrancy 
      • pre-excitation of ventricle 
    • Ventricular paced rhythm
    • Recording defect or artifact 
  • VT can give an impression of BBB
    • RBBB : even if typically VT does not present as RBBB do not close the diagnosis just yet 
    • Coumel's Tachycardia
      • Orthodeomic Tachyacarid with LBBB 
      • BBB now starts to conduct, causing shorter QRS on tachycardia 
  • How to differentiate
      • Rate and Hemodynamic stability ARE NOT factors
    • Brugada Algorithm for the differentiation
      • Precordial leads: 
        • RS in same side in all precordial leads
          • Every thing is positive in lead in QRS: VT 
        • R to S interval > 100 ms
        • AV dissociation
          • Capture beats and Fusion Beats : signifies AV dissociation. VT 
        • Morphology criteria for VT 
          • Morphology Criteria
            • RBB Morphology
              • True RB or not
                • Favors RBB:

                • Favors VT:
                  • First R bigger than r' (V1)
                  • >140 ms
            • LBB Morphology
              • True LB or not
                • Favors LLB
                • Favors VT
                  • Any Q or QS wave in V6
      • This has good sensitivity and specificity 
    • Other features to look into 
      • QRS: NorthWest axis : VT
Pathogenesis of Brugada vs LQT3 (that occurs with sleep)
  • Loss of function of SC5N (Sodium Channel): Brugada
  • Gain of function of SCN5: LQT3
Polymorphic VT

N Engl J Med 2012;367:1438-48

For V.T
  • Negative concordance in precordial leads
  • QRS > 160 msec
  • onset of nadir of S wave in V1longer than 100 msec
Against V.T 
  • No clear AV dissociation
  • EKG below shows the flutter wave at the same rate as VT above