Wide Complex Tachycardia

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. WIDE-COMPLEX 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  Accessory pathway (His PUrkinje system is bypassed) Anti-dromic ART (down the accessory pathway) A Fib with WPW  Understanding the preexcitation www.uptodate.com 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 Long QT Drug-Induced Prolongation of the QT Interval NEJM 2004 Long-QT Syndrome NEJM 2008 Catecholamine induced  Short Coupled Polymorphic VT (rare)  Typically, Verapamil is not given for VT, but in this case it is Verapamil sensitive VT  N Engl J Med 2012;367:1438-48 http://archinte.jamanetwork.com/article.aspx?articleid=2482345 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  http://archinte.jamanetwork.com/article.aspx?articleid=2482345