Monday, April 11, 2022

ECG Blog #297 — Is this VT?

The ECG in Figure-1 was obtained from an older man with a chief complaint of chest pressure and shortness and breath for the past several days. He was hemodynamically stable at the time the tracing in Figure-1 was recorded.
  • Is this VT (Ventricular Tachycardia)?
  • How certain are you of your answer?

Figure-1: ECG obtained from an older man with chest pressure and shortness of breath.

NOTE: For optimal clinical utility — I’ve divided my comments into 2 parts: i) My initial rapid assessment (that I completed within seconds of seeing this tracing); and, ii) My 2nd (more detailed) assessment of this tracing — with greater attention to specific ECG findings:
  • The “good news” — is that the patient in today’s case was hemodynamically stable at the time the ECG in Figure-1 was recorded. Therefore, by definition — this gives us at least a “moment of time” to assess the rhythm without need for immediate cardioversion. 

My Initial Rapid Assessment (Completed within Seconds! ):
By the Ps, Qs, 3R Approach (ECG Blog #185):
  • The rhythm is Rapid (clearly over 200/minute) — and Regular. The QRS complex looks wide (albeit not very wide) — and I do not see sinus P waves. Therefore — the rhythm in Figure-1 is a regular WCT ( = Wide-Complex Tachycardia), but without clear sign of atrial activity.
  • KEY Point: Even before looking at morphologic features — statistical odds are at least 80% that an older patient in a regular WCT rhythm without clear sign of atrial activity will turn out to be in VT. (These odds probably exceed 90% if this patient has underlying heart disease).

  • NEXT Step: I favor the 3-Simple Rules” for rapid distinction between VT vs SVT rhythms (See ECG Blog #196including the Audio Pearl in this post, for more on this topic). The fact that there is “extreme” axis deviation in Figure-1 (ie, an all negative QRS complex in lead aVF) — and an almost all negative QRS in lateral chest lead V6 — further increase statistical likelihood that this WCT rhythm is VT. That said — There are 2 ECG findings against this rhythm being VT: i) That QRS widening is minimal; and, ii) The initial portion of the QRS complex in multiple leads manifests rapid depolarization (ie, extremely steep S wave descent in virtually every lead with a predominantly negative QRS complex).

  • BOTTOM Line: Statistical likelihood (for this patient who is an older man) — that the regular WCT rhythm in Figure-1 will turn out to be VT is at least 90%. While it should be emphasized that 90% is not the same as 100% — We need to assume VT (and treat the patient accordingly)until proven otherwise.

More Detailed Assessment about Today's Case:
  • The rate of the rhythm in Figure-1 is extremely fast. There are a number of ways to rapidly estimate very fast heart rates (See ECG Blog #210and ECG Blog #278 for detailed illustration of my Every-Other-Beat Method). The R-R interval for today's rhythm is just over 1 large box in duration — which corresponds to a heart rate ~240/minute.

  • We are told that today's patient was “hemodynamically stable” at the time the ECG in Figure-1 was recorded. However, this patient is “older” — the ventricular rate of this WCT rhythm is extremely fast (~240/minute) — and the patient was having symptoms (ie, “chest pressure" and "shortness of breath”) at the time this ECG was recorded. This raises the question: Was this patient truly hemodynamicaly stable?
  • I have always felt that in such cases, “Ya Gotta Be There” in order to optimally assess hemodynamic stability (See ECG Blog #220for full discussion of this subject). While it may have been reasonable to initially opt for a trial of medical therapy — we need to recognize that at best, this patient’s “hemodynamic stability” is borderline. IF at any point during the treatment process the patient's condition worsens — prompt cardioversion will be needed.

  • It is sometimes difficult to accurately assess QRS duration at the bedside of a symptomatic patient in a very rapid arrhythmia. In Figure-1 — the QRS actually looks narrow in a number of leads (ie, in leads I, aVL, V1 — and in some of the leads with predominantly negative QRS complexes). Remember: QRS duration should be measured in that lead in which you can clearly see the beginning and end of the QRS complex — and in which the QRS looks widest! If we select lead aVR in Figure-1 — the QRS definitely looks wide!

  • It may also be difficult to assess atrial activity in rapid arrhythmias. We are looking for a number of different types of atrial activity: i) Are there sinus P waves? (ie, clearly upright P waves in lead II?); ii) Are there retrograde P waves? (ie, P waves that regularly occur after the QRS — and which are negative in the inferior leads, but positive in leads like aVR and V1?); iii) Are there "fib" waves? — "flutter" waves? — or other evidence of atrial activity?; and/or, iv) Do we see AV dissociation?

  • PEARL #1: Although the finding of AV Dissociation can provide strong support that a regular WCT rhythm is VT (See ECG Blog #217)it is very difficult to identify AV dissociation when the rate of the WCT rhythm is fast. In my experience, many clinicians think they see "AV dissociation" — when in fact, no reliably regular underlying sinus rhythm can be found. This may lead to misdiagnosis. It's best not to call AV dissociation unless you can reliably demonstrate (ie, with calipers) a reproducibly regular underlying sinus rhythm amidst the wide complexes of the tachycardia.
  • I do not see sinus P waves in Figure-1. I do not see clear evidence of retrograde atrial activity. The only possible indication of atrial activity that I see, is a small deflection following the QRS complex in lead V1. Given that I do not see this activity in other leads (and given that even if present, I cannot distinguish if this represents a positive or negative deflection) — I did not include this deflection in my assessment of the rhythm (because it does not provide diagnostic value).

  • BOTTOM Line: Even after more careful analysis — I was left with the same conclusion: Statistical likelihood that the regular WCT rhythm in Figure-1 will turn out to be VT is at least 90%. While 90% is not the same as 100% — We need to assume VT (and treat the patient accordingly) — until proven otherwise.

  • P.S. — If the rhythm in Figure-1 did turn out to be supraventricular (statistically unlikely — but possible) — I thought the most likely diagnosis would then be a reentry SVT rhythm (ie, AVNRT or orthodromic AVRT) — since AFlutter rarely presents with 1:1 AV conduction.

Follow-Up: The Case Continues:
The patient was treated with 1 dose of Adenosine without effect. Amiodarone was started — and several minutes later ECG #2 was obtained (bottom tracing in Figure-2).
  • How would YOU interpret the repeat ECG?
  • Does ECG #2 explain what the rhythm in ECG #1 was?
  •    HINT: Look closely again for atrial activity in both tracings!

Figure-2: Comparison between the initial ECG — and the repeat ECG after a dose of Adenosine and beginning Amiodarone.

The ventricular rate has significantly slowed in ECG #2 (from ~240/minute — to ~115/minute in ECG #2). The sawtooth pattern of AFlutter (Atrial Flutter) can now be seen in each of the inferior leads.
  • The rhythm in ECG #2 is AFlutter with 2:1 AV conduction. Since the ventricular rate is 115/minute — the atrial rate is 2X 115 — or about 230/minute.

  • Note that QRS morphology in each of the 12 leads in ECG #2 looks almost identical to QRS morphology in the initial tracing (except for the QRS looking slightly narrower in ECG #2).

  • What about atrial activity in both tracings? (See Figure-3).

Figure-3: I've magnified leads V1,V2 in both tracings — with focus on the appearance of atrial activity (See text).

The fact that QRS morphology is virtually identical in both ECG #1 and ECG #2 — confirms that the rhythm was supraventricular — and not VT.
  • Despite the final diagnosis — assuming the rhythm in ECG #1 was VT, and treating accordingly was the appropriate approach to initial management! We were not 100% certain about our diagnosis from Figure-1 — but we often have to begin management before knowing with certainty the etiology of the rhythm you are treating.
  • Treatment with both Adenosine and Amiodarone was appropriate in this case. The fact that the QRS complex was only minimally widened in ECG #1 suggests that IF the rhythm was VT — that it might be a form of idiopathic VT (ie, VT in the absence of underlying heart disease) — and some idiopathic VTs do respond to Adenosine (See ECG Blog #197). And if instead, the rhythm was supraventricular — then it should be either converted or temporarily slowed by Adenosine.
  • The advantage of IV Amiodarone as a treatment measure — is that it may effectively treat both ventricular and supraventricular tachyarrhythmias.

  • As to the question of atrial activity? — Slanted RED lines in the long lead II rhythm strip in ECG #2 highlight the 2:1 sawtooth pattern of AFlutter. Look at the RED arrows in lead V1 of this tracing.

  • Isn't the morphology of flutter waves (RED arrows) in lead V1 of ECG #2 the same as the morphology of the deflection highlighted by the BLUE arrows in lead V1 of the initial ECG?

  • PEARL #2: I did not initially realize that the deflection I was seeing in ECG #1 (BLUE arrows) represented 1:1 flutter activity! Sometimes the etiology of an arrhythmia will only become apparent after conversion to sinus rhythm, when you compare the "during" and "after" tracings. I found today's case fascinating — because it turns out that the initial rhythm in Figure-1 was AFlutter with 1:1 AV conduction! It is rare to see 1:1 AV conduction in a patient with AFlutter who is not on antiarrhythmic medication, and who does not have an accessory pathway.

  • PEARL #3: Despite a QRS morphology for the initial WCT rhythm in Figure-1 that strongly suggested the rhythm was VT (ie, extreme frontal plane axis — all positive QRS in lead aVR — almost all negative QRS in lead V6) — it turned out that the rhythm was supraventricular. Therefore — As helpful as QRS morphology may be for assessment of regular WCT rhythms — it is not perfect for distinguishing between VT vs SVT rhythms.

  • P.S.: Since we calculated the ventricular rate for the rhythm in ECG #1 to be ~240/minute — and since we determined this rhythm was AFlutter with 1:1 AV conduction — the initial rate of flutter waves was also 240/minute. Following IV Amiodarone — AV conduction decreased to 2:1 — and — the atrial rate of flutter waves was seen to decrease to ~230/minute (ie, 2:1 AV conduction, with a ventricular rate of ~115/minute).


Acknowledgment: My appreciation to 陳俊宏 (Chun-Hung Chen from Taichung City, Taiwan) for the case and this tracing.



Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
  • ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm.
  • ECG Blog #278 — Reviews one more example of how to quickly estimate a very rapid rate for this WCT rhythm.

  • ECG Blog #196 — Reviews another Case with a Regular WCT Rhythm. 

  • ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 

  • ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
  • ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the video ECG Media Pearl #21 in this blog post.

  • ECG Blog #220 — Case Study that reviews my LIST #1: Distinction between VT vs SVT with preexisting BBB or aberrant conduction. (Audio Pearl = How to determine IF your Patient is Hemodynamically Stable).

  • ECG Blog #211 — WHY does Aberrant Conduction occur?

  • ECG Blog #217 — Reviews the concept of how AV Dissociation may help in the diagnosis of VT (including the Audio Pearl in this post).


  1. Although one might dismiss it as semantics,don't you think an atrial rate of 230-240 is better called atrial tachycardia (150-250/min) and not atrial flutter?

  2. @ Subhasish — THANKS for your comment. There is a “gray zone” with heart rate between the limits for ATach vs AFlutter. In addition — there are many “atypical” AFlutters that simply cannot be distinguished from ATach from the surface ECG. That said — both the rate limits (untreated AFlutter most often manifesting an atrial rate between 250-350/minute vs <250/minute most of the time for ATach) — and morphology (ie, “sawtooth” of flutter vs the isoelectric baseline for ATach) — BOTH of these show overlap and less than perfect specificity in diagnosis. That said — the reason I said AFlutter (and not ATach) is that I thought each of the inferior leads in ECG #2 manifest such a perfect “sawtooth” pattern, that this had to be AFlutter. The atrial rate of 240/minute for the 1:1 flutter rate in ECG #1 I believe still IS within the range for untreated AFlutter. The atrial rate of 230/minute in ECG #2 is AFTER Amiodarone was given (which slowed the atrial rate a bit). THANKS again for your comment! — :)