Monday, December 23, 2019

Wide-complex tachycardia that didn’t follow the rules

Case contributed by Brooks Walsh, an emergency physician and ECG aficionado in Connecticut  (and a few comments by Smith)

A middle-aged patient came to the ED complaining of palpitations, dyspnea, sweating, and chest pressure that radiated to the arms. They had a history of non-ischemic cardiomyopathy (EF 30%), as well as PCI with one stent. Home medications included metoprolol, but no calcium- or sodium-channel blocking agents.

Initial ECG in the ED:

Presenting ECG: Wide-complex tachycardia at a rate about 200.

This is overwhelmingly likely to be ventricular tachycardia, even if only age and medical history are considered. If formal criteria for differentiating VT from SVT are applied, then VT appears even more likely. For example:
Lastly, the total QRS duration in V1, V2 is very long at 200 ms, longer than typical LBBB and again suggests VT.

An old ECG was checked:

Old baseline: Sinus rhythm with a LBBB
The RS duration is 100 ms, and the QRS width is 200 ms,
both markedly long for a LBBB

On one hand, the QRS in aVR in the baseline ECG is markedly different from that in the tachycardic ECG, again supporting a presumption of VT. 

Nevertheless, the widths of both the QRS complex and the RS duration are similar in both the old ECG and the tachycardia. This increased the likelihood that the wide-complex tachycardia was an SVT with a fixed LBBB.
Given some doubts about the ventricular origin of the WCT, the emergency physician elected to try adenosine first. A dose of 12 mg was properly administered, and no changes were noted on the monitor (at the time). The patient was then electrically cardioverted.

Post-conversion: Back to sinus with classic LBBB pattern

The WCT was presumed to be VT, and the patient admitted.

A surprise clue!

Although the emergency physician (along with an APRN and an RN) had not seen any alterations in the rhythm after adenosine was pushed, a paper recording of the episode was subsequently unearthed.

The WCT is interrupted by a series of variable-morphology QRS complexes, 
with atrial flutter waves note in II, III, and aVF.  

Detail of Flutter waves
The rate of the flutter waves matches the rate of the WCT (about 200/m), proving that the presenting WCT had been 1:1 atrial flutter. 

The subsequent EP study could not induce VT, only atrial fibrillation. Ablation to prevent recurrent flutter was performed.

This shows that, even if adenosine does not convert the rhythm, it can be useful in diagnosing the rhythm.

Spontaneous 1:1 atrial flutter

Atrial flutter usually has a rate of 300 F/m. The AV node, however, cannot conduct that rate, and typically will only permit 2:1 conduction, producing a usual ventricular rate of 150 bpm.

Atrial flutter conducting at 1:1 can be seen in certain contexts. For example, in a patient taking flecainide for atrial fibrillation, but not a beta-blocker.
Spontaneous atrial flutter with 1:1 conduction (i.e. in the absence of antiarrhythmic use) is rare, with only a handful of case reports in the literature: TanBurkhart, Murthy are 3 relatively recent open-access reports, while Nathwani is a abstract describing an unclear number of subjects with spontaneous 1:1 flutter with those with antiarrythmic-associated 1:1 flutter.

It isn't entirely clear why our patient developed 1:1 conduction with atrial flutter. Certain medical conditions (hyperthyroidism, accessory bypass tract, cathecholamine surge) can provoke it. Exercise can convert atrial flutter from 2:1 conduction to 1:1, apparently due to a combination of accelarated AV conduction and slowed flutter conduction. 

In our patient, the flutter rate of 200 is fairly slow, facilitating 1:1 conduction through the AV node. A slow flutter rate is not invariably associated with spontaneous 1:1 atrial flutter, however. Murthy, for example, described a healthy 50-year-old man who presented with a spontaneous 1:1 flutter at a rate of 280 bpm. 

In addition, the only study that compared spontaneous 1:1 atrial flutter with arrhythmic-associated 1:1 flutter found that the flutter was faster in spontaneous cases.

It makes sense the the atrial flutter rate would be faster in spontaneous cases, as there is not medication slowing that atrial rate, but it seems very unusual that the AV node could conduct at such a fast rate without some other condition (for instance hyperthyroidism).


It is well worth remembering that this was a rare case! 

In most middle-aged patients with a history of cardiomyopathy, a WCT will usually be VT. Furthermore, while specific criteria (e.g. precordial RS duration, aVR morphology) may not be perfectly sensitive, the are more likely to be helpful than suspecting 1:1 atrial flutter in patients not taking sodium-channel-blocking antiarrhythmics.

Comparison of the old and WCT ECGs might have suggested an SVT or atrial flutter at the time of presentation. However, it would not have been prudent for most clinicians to try e.g. a calcium-channel blocker as the first agent. When not absolutely sure, treat as VT!

Adenosine is safe in VT and may be useful in making the diagnosis.

MY Comment by KEN GRAUER, MD (12/23/2019):
It is ALWAYS great to welcome the contributions to Dr. Smith’s ECG Blog from Dr. Brooks Walsh — a highly skilled clinician + good friend and colleague who always stimulates conversation on important emergency medicine topics. Today’s case by Brooks is no exception.
  • I agree with many of the SUPERB clinical points emphasized by Brooks.
  • That said — I have a different opinion on several aspects of this case.
  • Definitive answers may be elusive — but my hope is to enhance Brooks’ presentation with important Learning Points for all.
  • BOTTOM LINE  I do not think ( = my opinion) that this wide-complex rhythm failed to “follow the rules”. On the contrary — I thought it followed the rules very nicely!
  • For clarity, in Figure-1 — I have put together and labeled ECG #1 ( = the initial ECG in this case, that was done in the ED) — with ECG #2 (which was the prior ECG found on this patient).

Figure-1: The first 2 ECGs shown in this case (See text). Although unfortunately there is no long lead II rhythm strip — RED arrows in ECG #2 highlight that sinus P waves (the rhythm is sinus bradycardia and arrhythmia) continue throughout the tracing, allowing us to establish with certainty the 7 sinus-conducted beats vs the 2 PVCs in this tracing. My comments below regarding QRS morphology pertain to the sinus-conducted beats in various leads.

I agree entirely with Brooks that ECG #1 shows a regular WCT ( = Wide-Complex Tachycardia) rhythmwithout clear evidence of atrial activity. Although I agree with Brooks that the rate is “about 200/minute” — I feel it important to be more precise with our rate estimation. This is EASY to do — by use of the Every-Other-Beat Method (CLICK HERE and listen to the next few minutes of my ECG Video for explanation of this easy-to-apply Method).
  • By the Every-Other-Beat Method — we can see in lead aVF of ECG #1 that it takes just over 3 large boxes on ECG grid paper (BLUE numbers) — to record 2 beats of the tachycardia (RED numbers). Therefore — HALF the rate, is just under 100 beats minute X 2 = ~190 beats/minute for the rate of the WCT in ECG #1.
I also agree entirely with Brooks that the overwhelming odds for this WCT rhythm without clear evidence of atrial activity favor VT as the diagnosis until proven otherwise! Statistical odds (given that this patient is at least middle-aged, with underlying structural heart disease in the form of a severe cardiomyopathy) that this rhythm is VT are >90% even before you look at the ECG! That said — disagree with the ECG findings selected as “supporting” evidence.
  • Having reviewed for over 3+ decades now all the predictive ECG criteria I have ever been able to “get my hands on” for distinguishing VT from Aberrant Conduction — I’ve developed “My Own Take” on this subject. This reflects my experience and my opinions — which I fully realize others may disagree with! (CLICK HERE for “My Take” on distinguishing VT vs SVT in the diagnosis of Regular WCT rhythms).
  • PEARL #1  Consider depending less on ECG criteria that are based on strict measurements — be this of QRS duration, R-to-S nadir, or other interval durations. This is because the boundaries of QRS onset, S wave nadir (lowest point of the S wave), and distinction between end of the QRS vs beginning of the ST-T wave are not always clear. It is one thing for expert cardiologists in a quiet office to retrospectively review a series of study tracings looking for incriminating measurements — and, another thing to be at the bedside of a crashing patient in a life-threatening tachyarrhythmia in which the speed of all around you is simply not conducive to decision-making based on precise measurements. In my experience — I’ve never been able to precisely measure R-to-S nadir, or QRS segments accurately enough to help during an emergency situation while at the bedside of a “crashing” patient.
  • PEARL #2  It is true that some delay of the initial part of the QRS complex (which I base on appearance rather than strict measurement) is more likely to be seen with VT than with supraventricular rhythms. But this information is best used (in my opinion) as a relative criterion — rather than an exact one. For example — the initial downslope of the S wave in the anterior leads of ECG #1 clearly manifests some delay (S wave downslope in leads V1-thru-V3 in ECG #1 is not a steep vertical line). Seeing this — I thought the slight delay I saw in R-to-S nadir could be consistent with VT — but most definitely was not diagnostic because of the CAVEAT I describe in the next bullet!
  • CAVEAT  All bets are off regarding the finding of initial QRS delay and marked QRS widening IF the patient has severe underlying structural heart disease — as baseline QRS morphology may be quite atypical when the patient has significant heart disease. For example — Note excessive fragmentation (notchingof the QRS complex in multiple leads in ECG #2 (especially in leads II, III, aVL, aVF, and V5). Fragmentation suggests scarring (ie, from prior MI and/or cardiomyopathy). It can therefore be seen from this patient’s prior baseline tracing ( = ECG #2) — that he had been in sinus rhythm with complete LBBB. Because of his severe underlying cardiomyopathy — his baseline QRS complex was extremely wide (attaining ~0.20 second for the sinus-conducted beats in lead V3 of ECG #2). In addition, there was marked fragmentation in ECG #2 — and that could contribute to a delay in R-to-S nadir times.
  • PEARL #3  IF you can be certain of the onset and offset of the QRS complex in lead aVR during a regular WCT rhythm — the finding of an entirely positive monophasic R wave in lead aVR is virtually diagnostic of VT. This is because, for the QRS complex to be all positive in lead aVR — the electrical impulse must be originating from the apex — and impulse origin from the apex virtually assures a ventricular etiology. In My Experience I have not found other QRS morphologies to be helpful in lead aVR. The DOTTED Black-and-White lines in ECG #1 represent my best effort to mark the onset of the QRS complex in all 12 leads in this tracing. I think (it is admittedly hard to be certain) that there istiny initial negative deflection before the positive deflection in lead aVR of ECG #1. (The fact that it is so difficult to determine the direction of the initial deflection in lead aVR of ECG #1 illustrates my reason for ignoring anything but an entirely positive QRS in lead aVR).
MInitial Assessment of ECG #1: I saw a regular WCT at ~190/minute without clear sign of atrial activity. The fact that this patient was middle-aged, and had a known severe cardiomyopathy meant statistically there was a >90% likelihood that this regular WCT rhythm was VT. QRS morphology was a bit atypical for LBBB in ECG #1 (all that notching + slight delay of anterior S wave downslopes) — but given the cardiomyopathy + a QRS morphology that could be consistent with LBBB (upright R wave in lateral leads I and V6 — and predominantly downward QRS in the anterior leads) — I could not rule out the possibility of an SVT rhythm.
  • Initial treatment with Adenosine was completely appropriate. Adenosine is unlikely to be helpful for ischemic VT — but, since QRS morphology in ECG #1 was potentially consistent with an SVT rhythm (with either underlying LBBB or LBBB aberration) — a “therapeutic trial” with Adenosine is exactly what I would have tried in this situation. The ultra-short half-life of Adenosine poses low risk of long-lasting adverse effects — and this drug may convert the rhythm if the etiology was an SVT.
  • If Adenosine is ineffective (as it was in this case) — then synchronized cardioversion becomes the treatment of choice.
  • PEARL #4  Emergency providers often think there are only 2 possible answers for the etiology of a regular WCT rhythm = either definite VT or definite SVT (in which the reason for QRS widening is either preexisting BBB or rate-related aberrant conduction). Remember that there is a 3rd possible answer = which is, that we may not be certain of the etiology of the WCT at this point in time. In this case — I favor a subjective relative probability estimate, based on my best educated guess. I’ve already suggested a ~90% likelihood that ECG #1 represents VT — but 90% is not 100%, and we need to remain open to other possibilities.
  • PEARL #5  There is no need to delay treatment of a regular WCT just because we are not 100% certain of the diagnosis. On the contrary — much (if not most) of the time, we begin arrhythmia treatment of a WCT before we know with 100% certainty what the rhythm is. Both Adenosine and synchronized cardioversion were appropriate initial treatments in this case!

Wwere then Shown ECG #2: I thought the appearance of the baseline tracing on this patient reduced the likelihood that the regular WCT in ECG #1 was VT.
  • As stated above — ECG #2 confirmed that this patient had a baseline wide QRS from complete LBBB + fragmentation in multiple leads.
  • Leads V1 and V2 in the baseline tracing previously showed delay in S wave downslope in this patient with LBBB — so this was not a “new finding” resulting from the wide tachycardia.
  • In addition — I was “struck” by the initial QRS deflection in leads II, III, aVL and aVF — which to my eye had a definite resemblance to the initial deflection in these leads during the WCT in ECG #1. Particularly in leads III and aVF — the resemblance was more than I’d attribute to chance.
  • BOTTOM LINE  After seeing ECG #2, I reduced my estimate that the rhythm in ECG #1 was VT to ~70-80%. This is still more-likely-than-not VT — but I was now less certain than I was before I had seen this patient's baseline tracing. That said, clinically it was time to treat this patient — and a definitive rhythm diagnosis was not essential for initial treatment measures!

That the regular WCT in ECG #1 was not VT was subsequently established — because EP study could not induce VT in the laboratory. Only AFib was induced during EP study.
  • That said — I do not agree that the rhythm strip recorded during Adenosine administration (which I show in Figure-2) proves that the rhythm in ECG #1 was 1:1 AFlutter.
Figure-2: The rhythm strip recorded during Adenosine administration (See text).

Reasons why I do not feel ECG #4 ( = the rhythm strip shown in Figure-2) proves that the rhythm in ECG #1 was 1:1 AFlutter include the following:
  • As previously discussed — the rate of the regular WCT rhythm was ~190/minute. This is different than the rate of flutter waves in ECG #4. By the Every-other-Beat Method — 2 flutter waves (RED numbers in the middle area of ECG #4) are recorded in less than the duration of 3 large boxes on ECG grid paper (BLUE numbers in this middle area in ECG #4). Therefore — HALF the rate for flutter waves is ~110-115/minute — which means that the rate of flutter in ECG #4 is ~220-230/minute, or significantly faster than the rate of the regular WCT.
  • Although difficult to see in ECG #4 because of all the ventricular ectopic beats (beats #7-thru-14 all manifest a different QRS morphology than was seen for beats #1-thru-6 during the regular WCT) — I do not see flutter waves in ECG #4 before beat #14. So rather than Adenosine “revealing” underlying AFlutter that had been conducting 1:1 during the regular WCT — isn’t it possible (if not more probable) that new-onset AFlutter after Adenosine was given may have been caused by Adenosine? (especially since the rate of flutter waves in ECG #4 is at least 30 beats/minute faster than the rate of the regular WCT)?
  • PEARL #6  It is important to be aware of the side effects of Adenosine. These include not only induction of significant bradycardia (albeit usually short-lived) — but also both ventricular and supraventricular tachyarrhythmias. Thus, Adenosine has been shown to induce both AFib and AFlutter — probably because of the effect this drug has on shortening atrial action potentials, and therefore reducing the effective refractory period in atrial tissue (Mallet ML: Proarrhythmic Effects of Adenosine — Emerg Med J 21:408-410, 2004).
  • That said — the fact that QRS morphology for beats #15 and 16 in ECG #4 (during the period of definite AFlutter) is very similar (minus superimposed flutter waves) in almost all leads to QRS morphology during beats #1-thru-6 (during the regular WCT) — strongly supports this QRS morphology as being supraventricular in origin — especially since the PR (or rather flutter-R) interval during AFlutter appears to be constant (the BLUE “PR” in ECG #4— which therefore suggests that flutter waves are conducted. (It would have been helpful to have a longer period of monitoring, in order to be more certain of the above observations ... ).

FINAL THOUGHTs: Our sincere THANKS to Dr. Brooks Walsh for presenting this fascinating case! It emphasizes a series of KEY concepts in emergency arrhythmia diagnosis and management. While statistically — VT was the most likely diagnosis for the rhythm in ECG #1 — a supraventricular etiology could never be discounted. In my opinion, the “rules” were followed — since it simply was never possible to be certain of the rhythm etiology until later during EP testing. Clinically, this did not matter — since appropriate initial treatment (in this case Adenosine, followed by synchronized cardioversion) was the SAME regardless of what the etiology of the regular WCT turned out to be.
  • Even though Adenosine did not convert the regular WCT rhythm — it did support our suspicion that the WCT was an SVT, because QRS morphology during flutter-conducted beats was virtually identical to QRS morphology during the WCT.
  • Availability of a prior (baseline) tracing — and a post-conversion tracing further supported a supraventricular etiology by revealing QRS morphology quite similar (albeit not identical) to QRS morphology during the tachycardia.
  • EP study was needed for confirmation of the final diagnosis.


  1. Dr. Walsh...

    Thank you for a very interesting and perplexing ECG. I assume the patient was hemodynamically stable since the physician began with adenosine. Finding the flutter waves was very fortuitous since RVOT tachycardias can look very similar to this and also terminate with adenosine. This can result in patients with VT being incorrectly diagnosed as SVT.

    You mentioned the patient had a non-ischemic cardiomyopathy. Do you know if there was significant dilatation? If so, an enlarged tricuspid annulus could have contributed to the slower flutter rate since it is the circumference of the tricuspid annulus that determines the flutter cycle length in most cases.

    In this case, extra sympathetic input due to his symptoms may have been enough to increase the conduction velocity through the AV node. The only thing that bothers me about that explanation is the fact that he appears to have a fixed 1st degree AV block at baseline. I'm not sure that any amount of adrenalin would overcome a fixed AV block.

    More to think about here...

    Congratulations on a well-managed and well-presented case.

    1. Thank you Jerry for your excellent (as always!) comment! I suspect you wrote BEFORE I added My Comment — so I’d welcome your thoughts on what I wrote. I only get to read these cases after they are published — and it took me a good many hours to put together my thoughts (and the above 2 Figures I added). As I was not privy to clinical details on this case — I decided “not to go there” regarding the important concept you raise — namely “adenosine-response” forms of VT. As you know, up to 10% of patients (could be more-or-less, depending on the population studied) have “idiopathic” VT (ie, VT without underlying structural heart disease) — and those are the VT forms that may respond to adenosine. I’d love to know more specifics on what the EP cardiologists in this case thought. I didn’t see proof from the ECGs we are given that flutter was the cause of the WCT. THANKS again for your thoughts! — :)

    2. Ken...

      I think you are right about the the flutter not necessarily being related to the initial WCT. Great observation! There are a couple of things about the initial presentation I'd like to mention:

      1) Age was mentioned as a consideration ("...likely to be ventricular tachycardia, even if only age and medical history are considered."). Never consider age in the diagnosis of a WCT. There isn't one algorithm that mentions it. A close friend of mine had his first episode of RVOT tachycardia at age 28. His cardiologist's son had VT at age 21 (I know the cardiologist personally) - both non-structural and neither requiring medication due to the short runs (2-3 seconds) and low frequency of episodes.

      2) Be careful comparing the QRS morphology at baseline with the QRS morphology during the tachycardia. While a similar bundle branch block pattern during baseline and WCT certainly SUPPORTS the diagnosis of SVT, it does not PROVE it. There is no reason on earth that a patient with a fixed LBBB cannot have a right ventricular tachycardia. Cardiomyopathy would also certainly complicate the diagnosis here. Only a bundle branch block pattern during WCT that is DIFFERENT than a baseline fixed BBB rules out SVT and PROVES VT.

      That was a really marathon analysis... Thanks!

      BTW, I found it interesting that toward the end of the rhythm strip (following the adenosine administration) there are PVCs from the left ventricle that are much narrower than the LBBB patterns. Any thoughts?

    3. THANKS for your comments Jerry! I use “AGE” selectively. As per your earlier point about “adenosine-responsive” forms of VT — as we’ve both said, younger (and “relatively younger”) adults when/IF they develop VT, are much more likely to manifest the idiopathic ( = non-structural) form of VT than an ischemic VT. Patients beyond “young adulthood” are more likely to develop coronary disease, therefore more likely IF they develop VT, to have an ischemic form of VT. So the AGE of a patient (as you say) clearly does not “rule in” or “rule out” a WCT as being VT — but it can alter relative probability of the “type” of a VT (which might influence your treatment approach) — realizing that MANY arrhythmias “never read the textbooks”. I also agree 1,000% with your comments regarding QRS morphology. For me, unless QRS morphology EXACTLY mimics the baseline tracing in ALL 12 leads — nothing is “ruled in” or “ruled out”. I was not privy to clinical follow-up in this case, and we did not see the EP cardiology report — so I simply accepted Brooks’ indication that EP cardiology “established the initial rhythm as an SVT”. Putting the “pieces” we did have together — I thought the resemblance (which was NOT identical) in various QRS morphologies, along with what seemed to be conducted flutter beats #15 and #16 in my Figure-2, supported the diagnosis of an SVT — but I agree completely that the limited period of monitoring on the ECGs we had do NOT unequivocably establish this rhythm diagnosis. In “real life” — I’d be there collecting a long enough monitoring strip until I attained more certainty about the rhythm diagnosis. As to your final query — I have no explanation about the relatively narrower PVCs other than the possibility that there may be distortion because the tracing in my Figure-2 is slanted and curved … THANKS again for all your thoughts! — :)

  2. The 1:1 conduction in this patient resulted because the flutter rate was slow, slow enough so that the AV node can conduct each atrial impulse, just as an ectopic atrial tachycardia with the atrial rate of about 200/m can conduct 1:1.
    K. Wang.

  3. Hi K! I believe My Comment (above) was probably written after you sent in yours. To my calculation (in my Figure-2) — the rate of flutter waves is different (ie, at least 30 beats/minute faster) than the rate of the rhythm during the regular WCT — therefore, I thought it unlikely that flutter was present the whole time (and conducting 1:1 during the WCT). Perhaps adenosine caused atrial flutter (which it can do)?

  4. Ken, no one can beat your meticulousness. Yes, the rate of the WCT in fig 1 is different from the atrial flutter rate in figure 4. The flutter rate may have been sped up from increased amount of circulating catecholamines due to adenosine given. Any way, I was pointing out that if the atrial rate in atrial flutter is slow enough, 1:1 conduction can result. The slowest atrial rate in atrial flutter in my collection was 150/m!!
    K. Wang.

  5. Ecg of the wct shows short R wave duration (<30 msec) in v2 which is in favour of svt. Also,in wct with lbbb morphology,onset of R to nadir of s >70 ms (and not 100 ms) is the criteria for vt, isn't it?

    1. @ Subhasish Singh — Yes, there is a thin initial r wave in lead V2 — and the R-to-Nadir time is <0.10 second. That said, there is no initial r wave at all in lead V1 — and the overall slope of the S wave descent in V1-thru-V4 is far LESS than vertical (ie, not overly rapid) — so although I completely agree with you that there ARE aspects of QRS morphology in ECG #1 that suggest a supraventricular etiology — to me ( = my opinion) — QRS morphology in ECG #1 is NOT at all definitive for a supraventricular etiology. As I discuss in My Comment above — I was initially undecided about the etiology of this WCT — although statistics did indeed favor VT ... THANKS again for your input! — :)

  6. 90% is not 100%. This post is rather educative! Are there Josephson sign in precordial leads, especially in V3 and V4?

    1. @ Unknown. Thanks for your comment. Josephson sign (notching near the nadir of the S wave) — seems to be present in anterior leads in the initial tracing. That said — I have never been a "fan" of this sign. Notching (fragmentation) tends to suggest "scar" — but this is a subjective sign, and HOW do we know what the baseline ECG looks like? I realize many quote this sign which is stated to have low sensitivity but high specificity — but I don't "trust" this sign ( = my opinion) — and I never use it. I realize others may disagree — and that's fine! — :)


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