Wide Complex Tachycardia

Intro

There’s an old adage that wide complex tachycardia is VTach until proven otherwise. While this is true as do not want to miss any potentially lethal arrhythmia, it is also important to understand the differential for wide complex tachycardias so that we can tailor our potential treatments to the specific arrhythmia. It is also important to note that in any unstable patient with a wide complex tachycardia (or narrow complex tachycardia) that electricity is always safe.

Differential

The differential for wide complex tachycardia can be broken down into the below groups:  regular and irregular wide complex tachycardias as well as toxic-metabolic syndromes.

Regular wide complex tachycardia is most common and often represents VTach. This group also includes antidromic AVRT and regular tachycardias with aberrancy. Aberrancy implies the patient has an EKG with baseline wide QRS (from a bundle branch block (BBB)). If an old EKG is available, the baseline wide QRS will be present. If the patient then develops tachycardia in the background of this BBB (e.g. SVT, sinus tachycardia, etc.), this will be seen as a wide complex tachycardia.

In much the same way, an irregular wide complex tachycardia is almost always from a patient who has a baseline EKG with a wide QRS complex who then develops an irregular tachycardia (e.g. Afib with RVR, AFlutter with variable block, etc.)

There is also a group of wide complex tachycardias caused by toxic metabolic syndromes that is discussed last in this post. This group often presents as a regular wide complex tachycardia but can also present as an irregular wide complex tachycardia. It’s also important to note that these syndromes can also present with HRs in the normal range depending on other factors. This group includes Na Channel blocker toxicity, hyperkalemia, and severe acidosis. 

Regular Wide Complex Tachycardia

Monomorphic Ventricular Tachycardia (VTach)

Monomorphic VTach is the most common type of VTach, and is often divided into non-sustained and sustained VTach. I’m sure we can all remember our sign-outs from the ICU of patients who had “few runs of non-sustained VTach.” This is defined as 3 beats or more of VTach lasting <30 seconds. We often get stat EKGs and electrolyte work-ups in these patients, and do a medication review for any arrhythmogenic medications (most often vasopressors or antiarrhythmics). Sustained VTach is defined as lasting >30 seconds or VTach requiring intervention due to hemodynamic compromise. VTach is often easy to recognize, however, a few notable characteristics on EKG include a broad QRS complex (often >160) with positive precordial QRS complexes (seen below). Management depends on stabilization with electricity vs. antiarrhythmic drugs as well as treatment of underlying cause. Causes can broadly be worked up using H+Ts but more often VTach is caused by cardiac injury (e.g. acute ischemia, old ischemic scarring, cardiomyopathy, electrolyte abnormalities, etc.)

Polymorphic Ventricular Tachycardia (VTach)

Polymorphic VTach is a type of VTach where there are multiple foci present in the ventricle conducting depolarization. This results in QRS complexes of varying size (amplitude), axis, and width of QRS complex (see example of Torsades below).

Torsades is what we most commonly think of when we hear polymorphic VTach, however, the most common cause is cardiac ischemia. Torsades occurs from prolongation of the QT and has many causes:  drugs (antipsychotics, antiarrhythmics, antiemetics, etc.), electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia), hypothermia as well as less common congenital causes (e.g. Jervell-Lange-Nielsen syndrome; Romano-Ward Syndrome). The reason prolonged QT is dangerous, and makes patients prone to VTach is the “R on T phenomenon”). This is the same phenomenon we try to avoid with synchronized cardioversion in tachyarrhythmic patients. In EKG below, we can see a patient with prolonged QT with R on T phenomenon.

Bidirectional VTach is another type of polymorphic VTach, and is most commonly seen with digoxin toxicity. It is a rare cause but can be considered in patients who are known to be taking digoxin. It presents as beat-to-beat alteration in the axis (seen below). 

Antidromic AVRT

This is a type of pre-excitation arrhythmia where depolarization conducts via an accessory pathway (Bundle of Kent) with retrograde conduction through the AV node. Since conduction occurs outside the AV node, it appears as a wide complex tachycardia. It often has a very fast rate (which can help differentiate it from other wide complex tachycardias) with rates often between 200 and 300. It can also be distinguished as can have delta wave (upslurring of QRS wave) and changing QRS morphologies.

It can be extremely difficult to differentiate antidromic AVRT from VTach. Luckily, electricity is safe in everyone. It is also safe to give these patients amiodarone, procainamide (med school answer), or ibutelide. Avoid AV blocking agents (adenosine, BB, CCBs).

Tachycardia with Aberrancy

Aberrancy refers to a rhythm with abnormal conduction. Most often it refers to a patient with a bundle branch block (BBB). If a patient has a BBB at baseline and they develop tachycardia, then this BBB will persist, and it will present as a wide complex tachycardia.

SVT with Aberrancy is one example of this. If a patient with a BBB develops SVT, then it will present as a wide complex tachycardia. If there is no prior EKG for comparison, it can be extremely difficult to differentiate these arrhythmias (LITFL: Differentiating VTach and SVT with Aberrancy). However, again electricity is always a safe option. 

Irregular Wide Complex Tachycardias

Atrial Fibrillation with Aberrancy

Similar to above, this is a patient with a baseline BBB, who then develops AFib with RVR. The BBB block persists leading to an irregularly irregular wide complex tachycardia. 

Atrial Fibrillation in patient with WPW

Patients with AVRT (e.g. WPW) can also develop atrial fibrillation. This is a WPW patient with a baseline EKG with the short PR interval and delta wave (upslurring QRS) who then develops atrial fibrillation on top of this disorder. This is relatively common in patients with WPW as they already have structurally irregular hearts. In fact, 20% of WPW patients may develop atrial fibrillation in their lifetime. If this does occur, it can result in an irregularly irregular wide complex tachycardia as we can imagine the chaotic atrial depolarizations now being able to travel down the accessory pathway (bundle of kent) without the stop light of the AV node as in typical AFib. These are the patients we definitely want to avoid AV blockers as they can lead to complete use of the accessory pathway (if AV node is blocked) and lead to circulatory collapse of the heart. Again, electricity is always a safe option.

 

Toxic Metabolic Syndromes

This is a group of disorders that can also lead to wide complex tachycardias. They are often regular wide complex tachycardias, however, they can also occasionally have an irregular rhythm as they are caused by toxic-metabolic syndromes:  hyperkalemia, Na channel blockers (TCA, antiarrhythmics, AEDs), and severe acidosis.

Amal Mattu gives a great lecture on this (Mattu Lecture on Youtube). Basically, he states toxic-metabolic syndromes should be on our differential for any really wide complex tachycardia. And by really wide, he means >200 msec (seen below). These syndromes also produce “slower” wide complex tachycardia (100-140 bpm) than is typically seen in traditional VTach. The reason this is so important to have on your differential is that if the ACLS algorithm is followed, one would give these patients amiodarone/lidocaine which have Na channel block properties which could further destabilize the patient if they in fact have hyperkalemia or Na channel blocker toxicity. Treatment for these patients rely on IV calcium and bicarbonate (great thing about these meds as well is that they are not harmful in VTach). Again, electricity is always safe.

I hope you enjoyed the post!