Written by Pendell Meyers, reviewed by Steve Smith and Scott Weingart
“Idiopathic ventricular tachycardias” refer to a group of tachydysrhythmias originating below the AV node and bundle of His but differing in etiology, prognosis, and treatment compared to classic ventricular tachycardia (VT). The name “idiopathic” is becoming more and more inappropriate, as various specific subgroups and specific etiologies are being discovered, including right ventricular outflow tract VT, fascicular VT, and bundle branch reentrant VT. To understand these entities one must first understand the differences between classic VT and idiopathic VTs.
Classic VT is by far the most common cause of wide complex regular tachycardia. It originates in (usually pathologic) myocardium, which is associated with advanced age, cardiovascular disease, structural heart disease and/or ischemia. Classic VT is associated with the prognosis of its underlying etiology, and is generally considered to have a significant rate of deterioration and hemodynamic compromise, largely due to the poor underlying myocardial function. On EKG, Classic VT tends to have longer QRS duration and a wider, less organized conduction morphology as compared with idiopathic VT, reflecting the key concept that classic VT does not usually originate in or near the intrinsic conduction system whereas many of the “idiopathic” VTs do. Unlike “idiopathic” VT, classic VT is more likely to show moderately specific signs such as AV dissociation, fusion beats, precordial QRS concordance, precordial R to S-wave nadir greater than 100 msec, R greater than R’ in V1, large upright R-wave in aVR, etc., however none of these are reliable in isolation.
Idiopathic VTs as a group are more commonly seen in younger, healthier patients than the typical classic VT patient, and are generally considered to have excellent prognosis with low rates of hemodynamic compromise and rhythm deterioration. These arrhythmias can be either automatic or reentrant in mechanism, and they often respond to antiarrhythmic medications that would ordinarily be ineffective or even contraindicated in classic VT. Idiopathic VTs can be better understood in their known subtypes, of which there are at least 3-4 at this time:
1) Right Ventricular Outflow Tract VT (RVOT VT)
Mechanism: triggered activity originating in the RVOT, which then accesses part of the nearby conduction system (thought to access the RBB within the septum).
Associations: Arrhythmogenic Right Ventricular Dysplasia
Variants: a similar arrhythmia has been described as originating from the LV outflow tract, with RBBB morphology with inferior frontal plane axis (RBBB + LPFB morphology). Response to treatment is unknown.
2) Fascicular Left Ventricular Tachycardia
Mechanism: Reentrant arrhythmia originating in or near specific parts of the intrinsic conduction system of the LV. There are at least three subtypes based on location, with the two most important being Posterior Fascicle VT (most common by far) and Anterior Fascicle VT.
Basic ECG Characteristics:
Posterior Fascicle VT: Precordial RBBB morphology with left axis deviation (or LAFB morphology) in the frontal plane
Anterior Fascicle VT: Precordial RBBB morphology with right axis deviation (or LPFB morphology) in the frontal plane
Treatment: Posterior fascicle VT is usually thought to be sensitive to verapamil. Anterior fascicle VT does not seem to have a consistently reported pharmacologic treatment.
Mechanism: Reentrant loop including at least one portion of the intrinsic conduction system. Unlike other idiopathic VTs, BBRVT is more often associated with underlying structural heart disease.
Basic ECG Characteristics: Depending on the bundles/fascicles involved and the direction of conduction, any combination of bundle branch and/or fascicular block morphology can be produced. The most common type reported seems to access the RBB anterogradely and the LBB retrogradely, causing the ECG to show LBBB morphology.
Treatment: This group of arrhythmias does not seem to have an effectively pharmacologic treatment. Neither adenosine nor verapamil have been reported to be consistently effective for these rhythms, however they are so rare that research is severely limited.
Risk of Hemodynamic compromise / rhythm deterioration
LV function on POCUS
General ECG Features of VTs, Idiopathic VTs, and SVTs with aberrancy:
Because the idiopathic VTs (unlike classic VT) frequently utilize the intrinsic conduction system, they are often indistinguishable from SVT with aberrancy due to morphology including bundle branch blocks and/or fascicular blocks. Differentiating classic VT from SVT with aberrancy and/or idiopathic VT is not the focus of this post (see posts like this one, this one, and this one), however there are some helpful rules of thumb worth mentioning here:
If the first portion of the QRS is conducted in a wide, disorganized, irregular way, then classic VT is by far more likely. If the first portion of the QRS is conducted in a rapid, steep, organized way, then this implies usage of the intrinsic conduction system, which takes place in SVT with aberrancy and many idiopathic VTs.
The ventricular rate of a regular wide complex monomorphic tachycardia cannot be reliably used to differentiate idiopathic from classic VT because the typical ranges are mostly overlapping and there are not really any reliable upper limits for either entity.
Most importantly: VT is by far the most common cause of wide complex regular tachycardia, and there is no perfectly reliable way to distinguish classic VT from idiopathic VT from SVT with aberrancy on the surface 12-lead ECG.
Prospective Differential Diagnosis and Treatment Plan based on ECG Features:
As EM physicians we rarely know the exact rhythm prospectively when we are standing in front of a patient with wide complex regular tachycardia. What we can do prospectively is identify QRS morphology that matches one of the following stereotypical patterns:
RBBB + LAFB (leftward frontal axis) Morphology
Rhythm differential includes classic VT, SVT with RBBB+LAFB, posterior fascicle VT, BBRVT, and probably other rare and obscure rhythms. If you believe it is one of the idiopathic VTs rather than classic VT or SVT with RBBB+LAFB, then posterior fascicle VT may be the most likely etiology. Posterior fascicle VT is usually sensitive to verapamil. However, one must consider the chance of giving verapamil inadvertently to to classic VT, which is formally contraindicated. Synchronized cardioversion (assuming you avoid shocking on the T-wave) is the only therapy which is both safe and effective among all etiologies in this category. Experts such as Dr. Smith might consider giving verapamil if electricity does not work AND the patient has very good LV function on POCUS, no history of cardiomyopathy, MI, heart failure, etc.
RBBB + LPFB (rightward frontal axis) Morphology:
Rhythm differential includes classic VT, SVT with RBBB+LPFB, anterior fascicle VT, BBRVT, LVOT VT, and probably other rare and obscure rhythms. If you believe it is one of the idiopathic VTs rather than classic VT or SVT with RBBB+LPFB, then anterior fascicle VT may be the most likely etiology. Anterior fascicle VT is thought to be somewhat less sensitive to verapamil than posterior fascicle VT, but there are some cases with reported efficacy. However, one must again consider the chance of giving verapamil inadvertently to to classic VT, which is classically contraindicated. Synchronized cardioversion (assuming you avoid shocking on the T-wave) is the only therapy which is both safe and effective among all etiologies in this category.
LBBB + Inferior frontal plane axis Morphology:
Rhythm differential includes classic VT, SVT with LBBB, RVOT VT, BBRVT, and probably other rare and obscure rhythms. If you believe it is one of the idiopathic VTs rather than classic VT or SVT with LBBB, then RVOT VT would be the most likely consideration in this category, which would typically be adenosine sensitive. This is convenient because adenosine is already indicated and recommended in our guidelines for stable, monomorphic, wide complex tachycardia. Again, synchronized cardioversion (assuming you avoid shocking on the T-wave) is the only therapy which is both safe and effective among all etiologies in this category. However, adenosine is also a safe, indicated, and less invasive strategy in this situation, as it will not harm a patient with classic VT.
Given the considerations above, I propose two options for your practice, with opposite points of view, both of which reflect a high degree of forethought and reflection on this topic.
First, as these patients are usually quite stable, see if you can find any previous records to shed light on the diagnosis, and any previous successes or failures of conversion attempts.
Option #1: Honey Badger
With this option you basically ignore the existence of these idiopathic VTs, ensuring that you can never make a mistake as a result of misdiagnosing a rhythm as idiopathic VT which in fact is NOT idiopathic VT. The reasoning includes:
“There are no reliable ways to differentiate idiopathic VT from VT, so I should always assume VT because this strategy is safer.”
“Even if I could prove it was an idiopathic VT prospectively, there is poor evidence correlating the EKG patterns with effective treatment, and some of the questionable treatments you’re advising have potentially negative side effects”
“The safest and most effective treatment for all the idiopathic VTs is electricity, so why go out of my way to diagnose something rare and less dangerous when the treatment will be the same regardless?”
“Even if I were correct about the diagnosis and possible treatment, if anything went wrong in any way and my reasoning had been based on treating idiopathic VT, how could I protect myself when none of the guidelines’ tachycardia algorithms deal with idiopathic VT?”
“Cardioversion is safe, effective, and fun.”
Option #2: Fancy Pants
In this option you adopt a practice in which you act on your experienced suspicion of IVT, but in a way that has been prospectively thought out to avoid the pitfalls and complications in the event that you’re wrong. You’ve thought out exactly when and why you’re going to use each medication. The reasoning includes:
Adenosine: “As long as the wide complex tachycardia is monomorphic and regular, adenosine is safe and guideline-approved for a stable patient, and assuming I am prepared for the ever-present chance of unexpected adenosine-induced rhythm deterioration just like I would in a narrow complex SVT conversion, then there cannot be any error attributed to considering FVT in this situation.” Dr. Smith would only give adenosine if RVOT is on the differential diagnosis, and that would be when there is RBBB pattern with inferior axis.
Verapamil: This medication is slightly more problematic, because of the 2015 ACLS Guidelines’ contraindication for verapamil/diltiazem in the setting of possible VT (Class III, Level of evidence B). There are some practitioners who believe that calcium channel blockers are likely safe after a high quality bedside ultrasound shows normal cardiac contractility. If you’re in that camp, then you could argue that your plan for suspected verapamil-sensitive FVT will be: 1) ensure good contractility by bedside US + chart review, then 2) give verapamil while being prepared for small chance of deterioration +/- prophylactic voodoo including fluid bolus and calcium, etc. Dr. Smith would always try electrical cardioversion first; however, it does not always work, or there is reversion to VT. In such a case, he would try verapamil, but only if ultrasound shows a high ejection fraction (good LV function).
“Sometimes electricity simply does not work. In these cases we must either rely on cardiologists to help or have an approach to these rare rhythms ourselves.”
“If the rhythm can be diagnosed and treated easily with only a single medication push, we can prevent unnecessary sedation and cardioversion, as well as any time/effort/complications that comes from it.”
“It is helpful prognostic and diagnostic information if the rhythm is successfully treated with adenosine/verapamil.”
Finally, many of these patients are rock stable and do not need to be converted right this second. If the easy method of electrical cardioversion is not working, it can be very helpful to get consultation from your friendly cardiologist or electrophysiologist. He/she may have some very good insights into the etiology of the tachycardia.