Saturday, April 2, 2022

An asymptomatic man in his 50s with heart rate in the 160s - what is the diagnosis? How will you manage this?

 Written by Pendell Meyers

A man in his late 50s with history of CAD with CABG, COPD, smoking, cirrhosis, and other comorbidities presented for an outpatient scheduled stress test which had been ordered for some exertional shortness of breath, palpitations, and presyncopal episodes over the past few months. When he presented to the office for the stress test, his screening vitals before any test or intervention were remarkable only for a heart rate of 160 bpm. He denied any symptoms whatsoever.

A 12-lead ECG was performed in the office:

What do you think?

The ECG shows a wide complex regular monomorphic tachycardia. I measure approximately 60-80 msec from QRS onset to R wave peak in several leads, with total QRS duration approximately 170-180 msec (computer QRS duration 182 msec).

Thus, the rhythm differential is VT vs. ST/SVT/Flutter with aberrancy. Even without further ECG expertise, VT is overwhelmingly more likely given age, cardiac history, comorbidities, sheer QRS duration, and simply the fact that VT is already more common than SVT with aberrancy even before historical information is considered.

The QRS morphology could be considered for RBBB and LAFB morphology, which could occur in SVT/ST/Flutter with RBBB/LAFB, idiopathic VT of the posterior fascicle, etc. 

I would assume it is VT until proven otherwise. Adenosine is perfectly safe and reasonable, but this is unlikely to be SVT, and thus I would not bother with it. If posterior fascicle idiopathic VT were being considered, verapamil could be a consideration, but would be potentially contraindicated in this patient with likely VT and known depressed EF.

If you are unfamiliar with the idiopathic VTs, read this:

Idiopathic Ventricular Tachycardias for the EM Physician

I would assume VT and treat as such.  Options are: 

1) Chemical (procainamide, amiodarone, etc.) or 

2) Electrical (sedation and synchronized cardioversion).

He was sent to the ED for evaluation.

Medics noted that the rhythm never changed during transport. The patient remained asymptomatic with otherwise normal vitals.

His ECG on arrival is seen here:

There are at least two capture/fusion beats seen among the wide complex regular rhythm, one seen in leads I, II, III, another seen in V1-V3.

We already suspected it was VT, and these fusion beats only further confirm that. However, please do not believe that fusion beats are absolutely accurate for diagnosing VT: 

Fusion Beat During Supraventricular Tachycardia: No criterion is absolutely accurate in differentiating wide complex tachycardia

Electrophysiology was consulted and recommended procainamide loading dose of 2 grams of procainamide over 2 hours, which was ordered (this is 12.5 mg/min, with a total dose of 14 mg/kg for this patient).

10 minutes after the procainamide infusion was started (after approximately 125 mg of procainamide), the patient remained asymptomatic but converted to this:

Conversion to sinus rhythm with RBBB (no clear LAFB or LPFB). Computer QT 498 msec, QTc 501. Computer QRS duration 150 msec.

The fact that the sinus rhythm has QRS with only RBBB (no LAFB) is another strong indicator that the original QRS complex during tachycardia was indeed ventricular (VT).

The patient was admitted for further workup. 

Echo was largely unchanged from prior, with known wall motion abnormalities, EF 45%. The cardiologist judged that the QT interval of approximately 500 msec corrected to near normal limits given the RBBB with QRS duration 150 msec.

The cardiologist interpreted this as "scar-mediated VT."

Sotalol was initiated for dysrhythmia prevention, with the plan to watch closely for worsening of COPD, or QT prolongation. Sotalol has both beta blocker and type III (potassium channel blockade) effects, meaning it directly prolongs the QT interval. Amiodarone was avoided due to COPD and cirrhosis. An ICD was implanted for VT with episodes of syncope. No further dysrhythmias occurred. The patient was discharged.

Procainamide is a class 1A sodium channel blocker, meaning it slows action potential propagation from cell to cell, reducing speed of conduction and prolonging the QRS and QT. Despite poor overall literature base, procainamide is typically considered the drug of choice for stable monomorphic VT after the results of the Procamio Study, which compared procainamide with amiodarone in the setting of stable monomorphic VT, and favored procainamide, showing roughly double the efficacy with half the adverse effects. Relative contraindications to both include a known prolonged QT, especially if the dysrhythmia is believed to be caused by prolonged QT.  

Another benefit: Procainamide is very effective at terminating SVT.  So if you are incorrect about your diagnosis, it might convert with procainamide anyway!

Check out RebelEM's post and podcast on the PROCAMIO trial for more:

Procainamide dosing:

IV loading dose is 10 to 17 mg/kg, typically administered at a rate of 20-50 mg/min.

Alternative dosing strategy is 100 mg every 5 minutes in adult patients until max dose of 17 mg/kg.

Another alternative dosing regimen was used in the Ottawa Aggressive Protocol (for chemical cardioversion of atrial fibrillation): 1 gm over 60 minutes.

The loading dose is given until the tachydysrhythmia is terminated, or the patient experiences hypotension, or QRS prolongation greater than 50% of baseline, or the max dose of 17 mg/kg has been given.

After the desired clinical effect is achieved, a maintenance dose is typically started at a rate of 1-4 mg/min.

Practice with these many other posts discussing VT vs. SVT:

Wide Complex Tachycardia: Lewis Leads Do Not Differentiate VT from SVT with Aberrancy

Learning Points:

The differential for a wide complex monomorphic tachycardia includes VT vs. ST/SVT/Flutter with aberrancy, all plus or minus hyperkalemia.

VT is simply more common than SVT with aberrancy, and VT is further more likely with increasing age, increasing cardiac history, and increasing QRS duration. There are many described methods attempting to differentiate SVT from VT, but none so far have shown sufficient efficacy and external validity. Assume VT when there is any doubt. Learn more if interested at the links above.

Procainamide is a good choice for chemical cardioversion of stable monomorphic VT.


1. Steil IG, Clement CM, Perry JJ et al. Association of the Ottawa Aggressive Protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation or flutter. CJEM 2010;12(3):181-91.

2. Komura S, Chinushi M, Furushima H. et al. Efficacy of Procainamide and Lidocaine in Terminating Sustained Monomorphic Ventricular Tachycardia. Circulation May 2010 Vol 72

3. Ortiz M et al. Randomized Comparison of Intravenous Procainamide vs. Intravenous Amiodarone for the Acute Treatment of Tolerated Wide QRS Tachycardia: the PROCAMIO Study. Eur Heart J 2016. PMID: 27354046


MY Comment by KEN GRAUER, MD (4/2/2022):


When Dr. Meyers showed me this case the other day — I literally begged him to post it as soon as possible. There are many Lessons to be learned!

For clarity — I'll reproduce and label the ECGs in today's case. ECG #1 was obtained in the office on a man in his late 50s, with a history of significant coronary disease

  • The patient reported a recent symptoms dyspnea on exertion of dyspnea on exert, palpitations and presyncopal episodes in recent months. Despite this — He was hemodynamically stable and absolutely asymptomatic at the time the ECG in Figure-1 was recorded.

Figure-1: The initial ECG in today's case (See text).

MY Thoughts on the Initial ECG:
The ECG in Figure-1 has to be interpreted as VT (Ventricular Tachycardia) — until proven otherwise! As I have discussed the user-friendly and time-efficient criteria I favor for distinction between VT vs SVT rhythms (with either preexisting BBB or aberrant conduction) — I'll refer those interested in more detail to My Comments in the May 5, 2020 and February 14, 2022 posts in Dr. Smith's Blog. Reasons why I'd estimate the likelihood of VT for the rhythm in Figure-1 at over 90% include the following.

  • The ECG in Figure-1 is a regular WCT ( = Wide-Complex Tachycardia) at ~160/minute, without clear sign of atrial activity. Pre-Test Likelihood that a regular WCT without P waves will turn out to be VT is ~80% in the literature. This figure goes up to ~90% Pre-Test Likelihood — IF the patient is "older" (ie, an adult of a "certain" age) — and if the patient has underlying heart disease. Therefore  Statistical likelihood that the regular WCT without P waves in Figure-1 will turn out to be VT is at least 90% even before we look at the actual ECG!
  • Because of this 1st bullet — We need to always assume VT for such rhythms until we prove otherwise, and treat accordingly. This does not mean that all patients need to be immediately shocked — but it does mean that since 90+% of such rhythms will turn out to be VT, that we need to assume VT until proven otherwise.

  • Now that we are looking closer at ECG #1 — reasons why statistical likelihood of VT goes up over 90% are: i) There is almost extreme axis deviation (ie, the QRS is all negative in lead III — albeit not all negative in lead aVF); ii) The QRS is very wide (ie, ~0.15 second); iii) There is delay in initial activation (ie, Note how wide the initial R waves are in leads V4, V5, V6); andiv) QRS morphology does not resemble any known form of conduction defect
  • It is this last criterion (ie, not resembling any known form of conduction defect) — that is the most suggestive of VT to me in today's case. Although there is superficial resemblance of QRS morphology to RBBB conduction (because of the upright QRS in lead V1 and the wide terminal S wave in lead V6) — the lack of any S wave at all in both high lateral leads (ie, leads I and aVL) — is distinctly against this representing RBBB conduction. The predominantly negative QRS in the inferior leads superficially resembles LAHB conduction — but most of the time (unless there has been a large prior inferior infarction) there will be more of an initial r wave in these inferior leads when the rhythm is supraventricular with LAHB conduction.
  • To Emphasize: Statistical odds of over 90% is not the same as 100% likelihood. There is almost always the possibility of exceptions (ie, prior infarction or cardiomyopathy that might result in a very abnormal baseline tracing). But over 90% likelihood is high enough to support the contention that the rhythm is VT until proven otherwise.

  • Lewis Leads: Use of another lead system is an easy-to-do but often forgotten application — that can be highly effective for revealing underlying atrial activity that was not evident on the standard ECG tracing (Please see my last Figure in the November 12, 2019 post of Dr. Smith's Blog for a reminder on how to apply Lewis Leads).

Lesson #1: Some Patients remain in VT for Hours (and even Days)!

I am aware of many cases of sustained VT in which the patient remained awake and alert for hours. I'm also aware a number of cases (including one at my former hospital) — where the patient was awake and alert in sustained VT for several days! So — Lesson #1 is that just because the patient is awake and alert with an excellent blood pressure does not mean that he/she is not in sustained VT. If the ventricular rate is not excessively fast — and the patient has preserved LV function — then it is possible possible to remain in sustained VT for hours, and even days.

  • The "good news" is that IF you patient is alert and stable in sustained VT — by definition this means that you do have time to try medical therapy (without need for immediate cardioversion) — as was successfully done in today's case.
  • The literature supports the premise that it is possible to remain in sustained VT for days (Symanski & Marriott — Heart-Lung 24:121,123, 1995). In this case report — the 69-year old woman (who incidently had a history of both coronary disease and cardiomyopathy) — remained in sustained VT for 5 days without hemodynamic deterioration. During this time, she was treated in the hospital with multiple antiarrhythmic medications including Adenosine, Verapamil and Digoxin. On her 5th hospital day — she was given Amiodarone, which successfully converted the rhythm. Luckily — she "survived" the above treatment course (as each of the first 3 drugs that were given could have been fatal, given their tendency to precipitate VT deterioration in the setting of severe underlying coronary disease).
  • To Emphasize: This case study by Symanski and Marriott is from 1995. Many advances in treatment have occurred in the 27 years since this article was published. That said — misdiagnosis of WCT rhythms for the same reasons cited by the authors remains all-too-common — so the lessons put forth in this 1995 article remain relevant. As I'll show in Figure-3 below — ample clues were present in the ECG of this patient to have confirmed VT — but they were ignored because providers didn't believe that anyone could remain alert and hemodynamically stable in sustained VT for as long as 5 days.

  • P.S.: One can only wonder for HOW LONG the patient in today's case had been living in sustained VT — since he was entirely unaware of his tachycardia (and his symptoms had been going on for some time!).

Lesson #2: This statement is WRONG: "Adenosine won't work in VT".
There are certain types of VT rhythms that are "adenosine-responsive". These include certain forms of idiopathic VT (ie, among the ~10% of patients with VT who do not have underlying heart disease). In particular — RVOT VT (Right Ventricular Outflow Track VT) — is responsive in some cases to Adenosine. 

  • The above said — Adenosine is highly unlikely to work with ischemic VT. Although most of the time — the ultra-short half-life of Adenosine will prevent deterioration of ischemic VT, use of this drug is not entirely safe in this setting. BOTTOM LINE — It's best not to use Adenosine if you suspect an ischemic form of VT.
  • In today's case — the patient has documented coronary disease and a QRS morphology that looks nothing like idiopathic VT. Adenosine should not be used in this situation. 
  • NOTE: Please see My Comment at the bottom of the page in the February 14, 2022 post in Dr. Smith's Blog for more on the topic of Idiopathic VT. For convenience — I've reproduced in Figure-4 in the Addendum below, a summary of this topic from this Feb. 14, 2022 post. 

The Initial ECG in the ED (ECG #2 in Figure-2):
I found ECG #2 to be fascinating (Top tracing in Figure-2).

  • QRS morphology for all but 2 of the beats in Figure-2 are the same as in the Office tracing that we saw in Figure-1.
  • Beats #4 and 15 look different! I Initially thought these beats represented ventricular "capture" and "fusion" respectively — which if true, would confirm the diagnosis of VT. And then I looked more closely.

  • It turns out that beats #4 and 15 are unlikely to be fusion beats! First — I see no indication of P waves anywhere in ECG #2. In addition, careful measurement (when you take the true beginning of each of these 2 beats) reveals that neither beat #4 nor beat #15 occur either early or late, as would be expected if there was ventricular "capture" or "fusion". Instead, these beats occur precisely on time with the other 23 beats in this tracing.
  • Support of my impression that beat #15 does not represent a fusion beat is forthcoming from: i) Cardiology assessment in this case that the rhythm in ECG #1 and ECG #2 represents scar-mediated VTandii) ECG #3 — in which the QRS complex is virtually all negative for beat #15 in lead V3 of ECG #2 — but virtually all positive in this same lead V3 after conversion to sinus rhythm in ECG #3. There is no way that fusion between the positive QRS in lead V3 of ECG #3 during sinus rhythm — could fuse with the nearly-all-positive QRS in lead V3 during the WCT rhythm in ECG #2 — to produce an all negative "fusion beat" looking like beat #15 does in lead V3 of ECG #2.

Instead of fusion and/or capture beats — I think it far more likely that precisely-on-time beats #4 and 15 in ECG #3 represent part of the same VT rhythm, in which there is a transient slight variation in the entrance and/or exit site of the VT circuit.

  • As per Martin et al (Circulation 11:e006569, 2018) — VT in the presence of underlying structural heart disease (such as coronary disease or cardiomyopathy) is dependent on reentry within scar regions. VT circuits in such patients are typically complex — and often manifest multiple entrance and exit sites. This may account for intermittent variation in QRS morphology during runs of VT in such patients.

Figure-2: The initial ECG in the ED — and the follow-up tracing in the ED after starting Procainamide (See text).

Lesson #3: How definite are Fusion Beats for proving VT?
I respecfully differ with Dr. Meyers' statement that no criterion is absolutely accurate in differentiating WCT rhythms. While true that many exceptions to the rules exist, and that most of the time you will not be 100% certain — there are occasions (in my experience) in which you can know that a rhythm is definitely VT.

  • As to the debate regarding whether a “Fusion” beat proves VT or not — my answer is, “It depends — but in the right circumstances, a fusion beat does prove VT”. I’m happy to debate this with others who may disagree with me.

  • In the case referenced above by Dr. Meyers (from the October 3, 2011 post in Dr. Smith’s Blog) — in which the EP cardiologist shows a different-looking QRS complex occurring in the middle of an SVT rhythm with QRS widening due to RBBB conduction — there is no atrial activity. As a result — there is no proof that the different-looking QRS complex is conducting from “above” (ie, that this different-looking beat is a sinus-conducted beat that was able to “get through” at just the right moment in a VT rhythm to fuse with a ventricular impulse). In addition — this different-looking beat in his example is wide! The simultaneously-recorded multi-lead rhythm strip also shows very large Q waves in leads II and III for this different-looking beat that are not present during the wide tachycardia — which means that IF this different-looking beat was supraventricular, and represented “fusion” with a VT rhythm — that the normal sinus rhythm would have to manifest even larger and wider inferior lead Q waves in order to produce an intermediate morphology. Although possible — this is unlikely. In my opinion — this October 3, 2011 example does not invalidate the specificity of true fusion beats.

  • BOTTOM LINE: It is well accepted that ventricular beats may occasionally be seen during a reentry SVT rhythm. If such ventricular beats do not penetrate the reentry circuit (which is not uncommon when the reentry circuit is contained entirely within the AV Node, as occurs with AVNRT) — then the reentry SVT rhythm will continue despite the presence of one or more ventricular beats that "break through". This is what apparently happened in the rhythm strip shown in the above noted Oct. 3, 2011 post. 
  • In order to demonstrate that a different-looking beat is a fusion beat that "proves" a ventricular etiology for the WCT rhythm you are interpreting — you need to see underlying on-time sinus P waves, which show a shorter-than-normal PR interval before the beat in question — and — you need to know what the normal sinus-conducted beat looks like — because a true “fusion beat” will manifest both QRS and ST-T wave morphology that is intermediate between the morphology of sinus-conducted beats and the wide beats you are trying to interpret.
  • I explain recognition and clinical use of Fusion beats for distinction between VT vs SVT in detail in ECG Blog #128.
  • For additional examples of what I would call “fusion beats” that truly prove that the wide rhythm that follows is VT — See ECG Blog #133 — ECG Blog #129 — ECG Blog #194 — and the May 5, 2020 post in Dr. Smith's ECG Blog.

I'll conclude my comments with Figure-3 — in which I show the ECG of the patient in the Case Study by Symanski & Marriott that I referred to earlier. Although the diagnosis of VT should have been evident from this tracing — this patient remained in the hospital, and was treated with drugs intended for SVT rhythms because no one believed it possible to stay alert and stable for 5 days in sustained VT.

Figure-3: In this Case Study by Symanski & Marriott — there is ample evidence that this regular WCT rhythm is VT. Note the extreme axis deviation in the limb leads (ie, all negative QRS in each of the inferior leads). QRS morphology does not resemble any known form of conduction block. RED arrows show definite P waves — with it being understandable why the BLUE arrow P waves are "hidden". Thus, there is AV dissociation — and the beat labeled "C" is a capture beat (preceded by a prolonged PR interval) — and "F" is a fusion beat.


ADDENDUM: I've added below in Figure-4 my summary on the Idiopathic VTs.


Figure-4: My summary regarding the Idiopathic VTs (taken from My Comment at the bottom of the page in the February 14, 2022 post in Dr. Smith's Blog).

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