Thursday, September 14, 2017

Wide Complex Tachycardia: is the patient stable or unstable?

Here is another case written by Pendell Meyers, a G2 at Stony Brook.  As I mentioned before, Pendell will be helping to edit and write the blog

Special thanks to Dr. Atif Farooqi who cracked this case for me.


A male in his 50s with history of "SVT with two prior failed ablations" presented for acute onset palpitations and shortness of breath. He appeared mildly short of breath and diaphoretic, but he was mentating perfectly, laughing about how many times he had been in this same situation. His initial automatic BP was 83/51, immediate manual pressure was 98/58.

Before we even get to his ECG, is he "stable" or "unstable"? This of course depends on your definitions, prior experience, and various other factors. If you care how the ACLS guidelines defines "stable vs. unstable", then prepare yourself for confusing and contradicting descriptions. 

ACLS defines unstable as "a condition in which vital organ function is acutely impaired or cardiac arrest is ongoing or imminent." (1)

Problem #1: Acute vital organ impairment is a definitively different level of instability compared to imminent or ongoing cardiac arrest. 
An asthma attack may constitute acute impairment of a vital organ's function, but clearly does not imply impending cardiac arrest.

They then give a list of suggested criteria which satisfy that condition, including terms such as "ischemic chest discomfort" and "acute heart failure." (1)

Problem #2: These terms have high interobserver variability
Unless it is the rare and obvious version of crushing chest pain in a clearly sick patient who is so diaphoretic the electrodes don't stick, how are we to agree upon what types of chest symptoms are "ischemic chest discomfort"? The majority of patients feel some sort of sensation in their chest with any rapid heart rate. Some insist that is is not pain, but rather "pressure," "discomfort," "throbbing," "tightness," or "fluttering." When ACLS warns about the patients with "ischemic" chest pain among all those with any chest symptoms, it seems that one is supposed to assume the worst, that the patient's chest discomfort is indeed ischemic. Similar confusion exists regarding what constitutes "acute heart failure" in the setting of tachycardia. 

The ACLS dichotomy is therefore both confusing and oversimplified. It does not account for the spectrum of variability seen in actual practice, and it does not help the clinician understand when to use electricity vs. less aggressive interventions for a tachydysrhythmia. Immediate electrical cardioversion is necessary when there is an imminent risk of deterioration. 

Proposed criteria which satisfy this restricted definition of unstable are:

  1. Acutely altered mental status or obtundation
  2. Overt signs of shock
  3. Acute heart failure causing pulmonary edema and severe respiratory distress which would otherwise require noninvasive or invasive positive pressure ventilation
  4. Sustained Polymorphic VT

Criteria 1-3 imply immediate risk of airway compromise, critical hypoperfusion, and/or critical hypoxemia. Additionally, traditionally first line interventions such as vagal maneuvers or adenosine in these cases are not feasible and/or risky, as the brief bradycardia or hypotension induced by these therapies may not be tolerated in the already tenuous hemodynamic state. In the setting of sustained PMVT, the rhythm itself carries an inherent risk of immediate deterioration and cardiac arrest, even in the momentary absence of the other criteria above. Polymorphic VT is a slightly more organized version of VFib and is treated identically, with unsynchronized defibrillation

A truly unstable adult patient whose instability is presumed to be caused by a tachydysrhythmia (other than PMVT) should undergo immediate synchronized cardioversion with 150-200 J under procedural sedation sedation. Sedation is unnecessary and dangerous if the patient is already obtunded. The monitor must be checked prior to every synchronized cardioversion to ensure that the machine is not syncing on the T-wave to avoid R-on-T phenomenon and rhythm deterioration. 

Back to the case:

Here is the patients presenting ECG:
What is your interpretation?

The first step in interpreting and managing tachyarrhythmias is classifying it according to two questions:

1) Narrow or Wide
2) Regular or irregular

This produces a limited differential for each category. More importantly, it offers an immediate empiric management strategy which will be safe and effective even without knowing the specific rhythm diagnosis within that category: 

Irregular rhythms can be further subdivided into "regularly" irregular or "irregularly" irregular. Irregularly irregular is completely chaotic and unpredictable, and is seen primarily with atrial fibrillation, but also with MAT and polymorphic VT. Regularly irregular occurs with sinus arrhythmia, sinus rhythm with variable AV block, PACs, PVCs, and atrial flutter with variable block. 

So what do you do when you're not sure if the rhythm is regularly or irregularly irregular?

Do not miss a truly irregularly irregular wide complex rhythm, because of the potential harms of any AV-nodal blockading medications in the setting of preexcited AF. Therefore if there is uncertainty, the clinician should assume an irregularly irregular rhythm and proceed accordingly. With that proviso, regularly irregular QRS complexes usually represent 

1) Single regular rhythm with constant or variable AV block
Examples: atrial flutter with variable block, sinus tachycardia with LBBB and rate-related RBBB, etc

2) Single regular rhythm with frequent premature beats
Examples: sinus rhythm with frequent PACs, sinus tachycardia with LBBB and frequent PVCs, etc

3) Two or more separate and competing rhythms
Examples: sinus rhythm with interjecting runs of VT or SVT, etc

This ECG shows a wide complex tachycardia which is overall irregular and has QRS complexes with differing morphology. Thus, the first consideration should be atrial fibrillation with WPW (preexcited AF), and this was my first impression. But there are sections of wide complex regular monomorphic rhythm within the tracing. AF can never be regular, so this cannot be AF with WPW. So you must break the ECG up into segments to understand what is happening. Here is the annotated ECG:   

There are two separate and consistent QRS morphologies in this ECG.  Black arrows demonstrate a QRS complex with distinct morphology, which appears each time before a run of regular wide complex tachycardia of different but also monomorphic QRS complexes (represented by the black line segments). 

The differential for the runs of regular monomorphic wide complex tachycardia is of course: VT, SVT with conduction abnormality, all plus or minus hyperkalemia. 

There are no features particularly worrisome for hyperkalemia. There are also no features that suggest obvious VT, such as concordance. If you thought the other distinct QRS complexes were possibly fusion beats or capture beats, then there should not have been a break in the rhythm just before them. Fusion/capture beats are described when one rhythm is constantly present before, during, and after the beat in question. Instead, this rhythm is repeatedly starting, terminating, and reoccuring. This makes short acting drugs like adenosine useless, because the rhythm will likely resume immediately after adenosine wears off.

Let's take a closer look:

In leads I, III, and V2, the QRS complexes marked with a black arrow can be seen to have a distinctly slow upslope, consistent with a delta wave. Thus, these QRS complexes may be supraventricular in origin with a delta wave or may simply be PVCs (in which case they are not delta waves). Either way, it seems as though the QRS complexes marked by arrows are initiating each run of monomorphic wide complex tachycardia. The reason these runs terminate is not exactly clear, but there is possibly an upright P-wave seen just after the last T-wave of each group (marked by red arrows). They do not appear to be retrograde P-waves.

There is no way to exclude VT based on this ECG, but presence of single QRS complexes with possible delta waves preceding regular tachycardia raises the suspicion of a regular reentrant rhythm using a bypass tract, such as atrioventricular reciprocating tachycardia (AVRT, see below). The beats indicated by black arrows initiate the AVRT, then it continues until something (possibly the atrial activity indicated by red arrows) terminates it, and it starts again.

Refresher on AVRT:

("Macroreentrant" is a large loop such as in atrial flutter, whereas "microreentrant" is a tiny loop such as seen in intra-nodal reentry in which the entire loop is contained within the AV node)

Atrioventricular Reentrant Tachycardia (AVRT) is a macroreentrant rhythm  involving the atria and ventricles, requiring an abnormal atrioventricular accessory pathway (also known as "bypass tract," "Bundle of Kent") in addition to the AV node. The accessory pathway may be able to conduct antegradely (from atria to ventricles), retrogradely (from ventricles to atria), or both, and these properties may also be transient and fluctuating based on various conditions. 

In sinus rhythm, the AP originates at the SA node and enters the AV node and the accessory pathway simultaneously (in parallel). Whereas the AV node normally has slow conduction (causing the delay between the P-wave and the QRS), the bypass tract does not, and depolarization through the bypass tract begins first (“preexcitation”). Because the bypass tract does not connect directly to the specialized conduction system, the impulse traverses slowly through myocardium. Since slow conduction creates a wide QRS complex, this results in a wide initial deflection known as a “delta” wave. When the AP from the AV node transmits down through the conduction system, it rapidly converges with the AP from the bypass tract. This manifests as a fusion beat with the initial part of the QRS abnormal (delta wave) and the latter part appearing more normal.

An appropriately timed premature contraction may find one pathway refractory while the other is able to accept the premature impulse. By the time the AP arrives at the other pathway, it has fully repolarized and can continue the circuit in series. The macro-reentrant loop may proceed in an orthodromic (anterogradely down the AV node and retrogradely up the accessory pathway) or antidromic (opposite) fashion. Orthodromic AVRT activates the ventricles using the intrinsic conduction system, resulting in QRS morphology identical to the patient’s baseline (unless rate-related BBB is present). Antidromic AVRT involves the spread of conduction through the myocardium without using the intrinsic conduction system, resulting in a WCT which is often indistinguishable from VT.

See this diagram for explanation of the waveforms created by the presence of the bypass tract:

When AVRT results in a narrow rhythm, it must have accessed the intrinsic conduction system antegradely (usually via the AV node), and is termed orthodromic AVRT. When the QRS complex is wide as in this case, it is either antidromic AVRT (accessing the ventricles via the bypass tract) or orthodromic with conduction abnormality despite using the conduction system (BBBs, Non-specific IVCD, hyperK, Na channel blockade).

Case continued

No prior ECG was available, and no prior medical records were on file. Medics reported they had attempted adenosine 6 and 12 mg en route with no perceived change in rhythm. The patient was presumed to be symptomatic from the rhythm, and had concerning vital signs and physical exam features, but it seemed clear to the providers at that time that he was not at risk for impending cardiac arrest. 

The rhythm was thought at the time to be an irregularly irregular wide complex rhythm, because the patterns above were not yet recognized. 

Amiodarone infusion was ordered. (If your patient actually has AF with WPW, this could be dangerous! Like adenosine, amiodarone may not be safe in AF with WPW. Its beta blocking effect could result in rhythm deterioration, and it is thus contraindicated in the ACLS and SVT guidelines for any irregular or polymorphic wide complex tachycardia). (1,2)

45 minutes after the infusion was started, the patient became progressively more hypotensive (~80/40) and less alert despite no change in the rhythm. He underwent sedation and electrical cardioversion, which immediately produced this ECG:

Sinus rhythm with distinct delta waves. This further supports the suspicion of intermittent runs of antidromic AVRT. The QRS morphology does not appear to match the singular beats marked by black arrows in the prior ECG.

The patient's mental status and vitals quickly normalized, and the rhythm did not recur. Normally, cardioversion or short acting medications would not solve this problem because the recurring rhythm should simply recur immediately after therapy (this is why longer acting medications are indicated in this scenario). Amiodarone acts via multiple mechanisms, and could potentially be stopping the initiation of AVRT by preventing PACs or PVCs (labelled by red arrows above). Cardiology was consulted, and the patient was admitted to undergo an EP study.

Here is the report of the ED study:

"The patient presented to the lab in NSR, antidromic AVRT was induced with catheter manipulation which degenerated into AF requiring multiple cardioversions. The patient never stayed in AVRT long enough to permit full diagnostic maneuvers. There was no retrograde bypass tract conduction. Mapping of earliest antegrade activation was performed during atrial pacing, the R posteroseptal area had some early sites but ablation was unsuccessful. Mapping the MV annulus revealed an early site that resulted in loss of preexcitation with bumping, when preexcitation returned ablation at this site resulted in permanent loss of preexcitation at 1.4 seconds into the first ablation lesion."

Thus, the patient had apparently successful ablation of a left posteroseptal bypass tract. 

Here is his post-procedure ECG:

Normal sinus rhythm with no delta waves.

He has been free of palpitations and arrhythmias for over 1 year. 

Learning Points:

  1. Stable vs. unstable is not well defined by the current ACLS guidelines, but the clinician should be able to recognize the signs of impending deterioration and change management accordingly
  2. When a wide complex rhythm is not perfectly regular and also not irregularly irregular, one should consider AV blocks, premature beats, or multiple competing/alternating rhythms, while keeping in mind the risks of missing an irregularly irregular wide complex tachycardia
  3. Antidromic AVRT is a rare condition which causes regular wide complex monomorphic tachycardia that can be indistinguishable from VT or hyperkalemia-accompanied arrhythmias



  1. after the cardioversion the arrhythmia did nor reccurr but if it did what would be the drug of choise ??

  2. Procainamide would be supported by the currently held physiology and the AHA/ACC guidelines in this case. Ibutilide is also listed with the same level of recommendation in our guidelines (Class I, Level C-LD: very low level of evidence, but supposedly more than just expert opinion), but unless I'm mistaken this drug is more expensive and less commonly used.

    Electricity is clearly not going to be effective long term if the rhythm is re-initiating after cardioversion. AV nodal blockers (including amiodarone) are contraindicated because of the presence of the accessory pathway, even if the rhythm is not currently AF with WPW, because of 1) the small chance we might have been wrong about the rhythm to begin with and 2) the chance of conversion to AF spontaneously or with other therapies, which is not uncommon.


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