Wide complex tachycardias

Overview
Wide complex tachycardia or WCT refers to a cardiac rhythm of more than 100 bpm with a QRS duration of 120 ms or more on the surface electrocardiogram.

Definition
Heart rate >100 with QRS duration >120ms.

Background

 * Wide complex tachycardia (WCT) can be either:
 * Supra ventricular tachycardia (SVT) with aberrancy
 * Ventricular tachycardia (VT)
 * Antegrade conduction down an accessory bypass tract.
 * 80% of WCT will be VT. 98% will be VT if structural heart disease is present. 7% of patients with SVT will have prior myocardial infarction (MI).

Differential Diagnosis

 * Regular
 * VT (slight irregularity of RR)
 * SVT with aberrancy: Sinus, atrial tachycardia (AT), or Flutter.
 * Antidromic atrioventricular reentrant tachycardia (AVRT)
 * Irregular
 * First 50 beats of VT
 * SVT with aberrancy: Atrial fibrillation, multifocal atrial tachycardia (MAT)
 * Atrial fibrillation with bypass tract
 * The mechanism of SVT with aberrancy is usually concealed retrograde conduction. The ventricular beat penetrates the right branch (RB) or left branch (LB).  When the next supraventricular activation front occurs that bundle is refractory and if conduction can occur, it will proceed down the other bundle.  Since the RB has a longer refractory period than the LB, a right bundle branch block (RBBB) morphology is more common.
 * Other mechanisms of “rate related aberrancy” are preexisting bundle branch block (BBB), physiologic (phase 3) aberration and use dependent aberration secondary to medication. In physiologic aberration, the stimulus comes to the His-Purkinje system before it has fully recovered from the previous stimulus. The ensuing activation is either blocked or conducts slowly.  Again, the RB is the one more at risk.  Most commonly seen at the onset of paroxysmal supraventricular tachycardia (PSVT), but can become sustained.
 * In use-dependent aberration, a patient on and anti-arrhythmic (especially Ic agents) will have a progressive decrement in ventricular conduction rate the more it is stimulated. During faster heart rates, less time is available for the drug to dissociate from the receptor and an increased number of receptors are blocked.

Differentiation of VT from Antidromic AVRT

 * Angina pectoris (AP) activate ventricles from base to apex by virtue of their location in the atrioventricular (AV) ring. This results in predominately positive QRS complexes in V4-V6.  If negative, favors VT.  For same reason, qR complexes in V2-V4 cannot be found in AVRT unless there is preexisting heart disease.


 * Because the atria are part of the circuit in AVRT, any relationship other than 1:1 of P and QRS means VT (100%).

Algorithm

 * 1) If polarity of V4-V6 is negative, then VT (100%).
 * 2) If qR present in V4-V6, then VT (100%).
 * 3) If 1:1 AV relationship not present (more QRS than P), then VT. (100%)
 * If none of above present, 25% will still be VT

History and Symptoms

 * Age
 * Presence of preexisting heart disease
 * Duration of symptoms
 * Medications

Physical Examination

 * Vitals to assess hemodynamic stability
 * “Cannon-a waves” (a manifestation of AV dissociation)
 * Carotid sinus massage (CSM)/Valsalva: ST can gradually slow. MAT, AT, Flutter, and AF may transiently slow. An AV nodal dependent WCT may terminate.  AV dissociation may become more apparent with CSM in VT. VT can terminate with CSM

Electrocardiogram

 * Extreme axis deviation favors VT. Especially -90 to -180 or “northwest” or “superior” axis. (23% of SVT will have SAD)
 * QRS duration >140 msec favors VT (21% of VT will have QRS <140 msec)
 * AV dissociation is demonstrated in only 21% of VT
 * Morphologic Criteria
 * 4% of SVT and 6% of VT did not fulfill criteria in any lead
 * 40% will have discordance between V1/V2 and V5/V6. One lead may suggest VT while another suggests SVT.
 * An algorithmic approach was proposed by Brugada in 1991. It has a reported sensitivity of  99%  and specificity of 97%.

Acute Pharmacotherapies

 * If stable: (More patients than you think)
 * DO NOT USE Ca2+ Channel blocker, Digoxin or Adenosine if you don't not know the etiology of the Wide Complex Tachycardia. Ca2+ Channel blockers and Digoxin can lead to accelerated conduction down a bypass tract and VF.
 * Though ACLS guidelines recommend a diagnostic trial of Adenosine, it can precipitate VF in some patients with SVT. Patients who have underlying coronary disease may become ischemic from coronary steal. Rhythm can degenerate and lead to VF that cannot be resuscitated. Furthermore, some VT (esp those with structurally normal hearts) are adenosine responsive and can terminate.
 * Etiology Uncertain
 * Pronestyl 15mg/kg load over 30 minutes then 2-6mg/min gtt
 * Ventricular Tachycardia with active ischemia
 * Lidocaine 1 mg/kg q5-10 min up to 3 times then 2-6mg.min gtt
 * If unsuccessful, Pronestyl as above
 * If unsuccessful, IV Amiodarone 150-300 load over 15-20min. 30-60mg/hr gtt for total of 1gram
 * Ventricular Tachycardia in Setting of Cardiomyopathy
 * Skip Lidocaine and go straight to Pronestyl
 * Positively SVT with aberrancy
 * Adenosine 6mg rapid IV bolus in large vein. May repeat with 12mg x2.
 * Lopressor 2.5-5.0mg IV
 * Diltiazem 10-20mg bolus followed by gtt 5-20mg/hr
 * Verapamil 2.5-5.0mg bolus.
 * Avoid Digoxin. Takes too long to work and can be proarrhythmic
 * Pronestyl as above
 * Antidromic AVRT
 * If 100% positive AF is not underlying, can terminate with a nodal blocker
 * If unsure, Pronestyl as above
 * Pearls from MEJ
 * In right bundle branch block (RBBB) morphology with normal or inferior axis, R/S ratio may be >1 in VT or <1 in SVT
 * If QRS during tachycardia is narrower than in normal sinus rhythm (NSR), suggests VT

Surgery and Device Based Therapy

 * Hypotension with symptoms, chest pain, congestive heart failure (CHF), seizure etc.: Defibrillate