Tachycardia in cardiology clinic, what is the rhythm?

Submitted anonymously, written by Willy Frick

A man in his 70s with a history of remote MI (details unavailable) and prior stent placement presented to cardiology clinic for routine follow up. He complained of days to weeks of palpitations and dyspnea. His clinic ECG is shown.

What do you think?

In an elderly patient complaining of palpitations, we have an ECG with heart rate 140 bpm. This is an arrhythmia until proven otherwise. The first step is in defining the atrial activity. The best leads for atrial activity are typically leads V1 and II, although individuals may vary. Inspecting V1 for atrial activity, there is nothing convincing for sinus activity. The second beat is preceded by a possible sinus beat, but it does not seem consistent.

Looking at lead II, there is a small deflection before the QRS. You might wonder if this is a P wave.

However, if you draw a vertical line to compare to neighboring lead I, you see that this is actually part of the QRS!

The slurred onset in lead I is suspicious for pre-excitation. But even in a pre-excited SVT, there will be some atrial activity. Can we find it?

Have another look at the V1 rhythm strip below and see if you can find any evidence for atrial activity before reading further.  (As always, click on the image to enlarge it!!)

With close inspection, you may notice a few unusual waveforms. I've pointed out some of the most believable candidates for atrial activity.

This raises the possibility of AV dissociation. A good way to test this is to use calipers to march out the P waves in both directions. Remember that sinus activity is not always perfectly regular. It can vary slightly from one beat to the next.

Allowing for a little bit of this fudge factor, we can pick two of the closely spaced arrows above and march them in either direction to get the following figure:

Some of the caliper tips fall in the middle of QRS complexes where it would be impossible to appreciate a buried P wave, but otherwise they march perfectly with irregular deflections in the waveform! This is a critical finding. This proves AV dissociation, and by extension ventricular tachycardia.

The cardiologist evaluating the patient in clinic did not recognize this. The note lists a diagnosis of "tachycardia," which is described as "narrow complex." (The QRS duration is approximately 144 ms, certainly not narrow.) The note says vagal maneuvers were unsuccessful, and recommends evaluation in the ER. The note says the patient's wife will drive him to the ER.

Repeat ECG obtained in ER:

Fortunately for the patient, his ventricular tachycardia spontaneously resolved. The current ECG shows sinus tachycardia with old inferior infarct. (Strictly speaking, the clinic ECG also had sinus tachycardia underneath the ventricular tachycardia.) He was admitted to cardiology. Serial troponin was undetectable. Documentation lists a diagnosis of "sinus tachycardia."

As an aside, sinus tachycardia at a rate of 140 in an elderly man is seriously concerning and demands an explanation. This would be approximately 95% of the patient's maximum predicted sinus rate. This demands an explanation -- sepsis, hemorrhage, withdrawal, etc. Calling sinus tachycardia raises more questions than answers.

After ruling out for ACS, the patient underwent angiography where he was found to have severe stable disease, which was already known. He was discharged with a plan for outpatient PCI to his chronically occluded RCA. There was no mention of ventricular tachycardia.

Fortunately for the patient, the person who submitted this case discovered it while reading ECGs. The submitter started the patient on amiodarone and arranged implantation of a defibrillator.

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MY Comment, by KEN GRAUER, MD (12/27/2024):

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Superb discussion by Dr. Frick in today's case, that highlights a series of important points regarding the ECG recognition of stable VT (Ventricular Tachycardia). I'll add the points that I note below.

• For clarity and ease of comparison in Figure-1 — I've labeled and have put the two 12-lead ECGs from today's case together.

For How Long can a Patient remain in Stable VT?

Today's case is remarkable in that this man in his 70s with a known history of prior MI and prior stent placement was misdiagnosed as having an SVT (SupraVentricular Tachycardia) by a cardiologist. Vagal maneuvers were tried — but were unsuccessful.  The patient was then sent to the ED for evaluation not by ambulance — but driven to the ED by his wife. And all the while — this patient was in stable VT!

• By history (since this patient had complained for days-to-weeks of palpitations and dyspnea) — it is possible that this patient could have been in stable VT for days-to-weeks!
• 2 major factors most probably led to the misdiagnosis of today's arrhythmia: i) This patient's history was over an extended period of time (ie, palpitations over a period of days-to-weeks); — and ii) This patient was hemodynamically stable throughout initial evaluation by his cardiologist (including during the performance of vagal maneuvers).
• As I've noted on a number of occasions in Dr. Smith's ECG Blog (See My Comments in the posts from September 20, 2023 — January 10, 2024 — and April 2, 2022 to name just a few) — 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. 
• The LESSON is clear: Just because a patient remains awake and alert with an adequate blood pressure for an extended period of time — does not rule out the possibility of sustained VT. If the ventricular rate is not excessively fast (such as ~140/minute for today's initial ECG) — and the patient has reasonable LV function — then it is possible possible to remain in sustained VT for hours, and even days.
• The literature supports the premise that it is possible to remain in sustained VT for days at a time (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). NOTE: Although this case study is from 1995 — the misdiagnosis of wide tachycardias "because the patient is stable" remains all-too-common in 2025.

The Importance of Statistics and QRS Morphology:

The fact that the older man in today's case has known coronary disease — means that even before looking at his initial ECG — statistical odds that his regular WCT (Wide-Complex Tachycardia) rhythm will be VT are at least 90%.

• These statistical odds that the rhythm is VT can be further increased by noting the following in ECG #1: i) QRS morphology is not typical for any known conduction defect (ie, Instead of predominant negativity in the chest leads with LBBB until at least lead V4 — the QRS shows definite positivity already by lead V2); — and, ii) Instead of a rapid initial depolarization vector (as is so often seen with SVT rhythms) — the initial QRS depolarization vector is delayed (as well as fragmented) in multiple leads (such as leads III and V2-thru-V6).
• NOTE: The only exception that might account for the unusual QRS morphology seen in today's initial ECG — might be if a prior baseline ECG in sinus rhythm could be found showing the same unusual QRS morphology. Given that this patient was initially seen and treated (undergoing vagal maneuvers) in cardiology clinic — there may have been time to quickly find a patient record with a previous ECG in sinus rhythm.

What to Know about AV Dissociation:

Dr. Frick skillfully reviews in sequential detail the steps he followed to identify AV dissociation in ECG #1. As he emphasizes — defining the existence of an underlying independent atrial rhythm proves that the other rhythm in this tracing that manifests regular but wide QRS complexes must be ventricular in etiology.

• KEY Point: In my experience of meticulously searching for AV dissociation in every WCT rhythm I have encountered over a period of decades — it is rare to find it! Unfortunately, the desire of wanting (hoping) to "see" AV dissociation often leads emergency providers astray.
• The reality is that definitive diagnosis of VT is not nearly as difficult when the rate of the WCT rhythm is not overly fast. This is because diagnostic fusion beats and AV dissociation are much more likely to be seen in these relatively slower ventricular rhythms. The problem arises with relatively faster WCT rhythms — because underlying regular atrial activity so often gets hidden within wide QRS complexes and wider accompanying ST-T waves.
• My Experience: Most cases of supposed "AV dissociation" that I have seen others identify — turn out to be artifactual "blips" rather than true AV dissociation. This is important — because IF you are able to truly identify AV dissociation (as Dr. Frick does in today's case) — then you have definitively diagnosed VT. But if you only think that you may be seeing AV dissociation in a regular WCT rhythm — then it is best not to include this information in your assessment because it is much more likely than not to misguide you.
• PEARL: It is best not to diagnose AV dissociation unless you are 100% certain of this finding. And, the only way you can be 100% certain there is AV dissociation — is if you are able to walk out underlying independent regular atrial activity through at least a substantial portion of the rhythm strip. Finding 2, 3 or 4 "blips" that do not walk out further is not "proof" of AV dissociation.

Before I read Dr. Frick's description in today's case — I also suspected AV dissociation. This is because despite all of the fragmentation of QRS complexes that we see in ECG #1 — the overall tracing is surprisingly "clean" without significant artifact. This is why I suspected those small negative deflections that we intermittently see throughout the long lead V1 rhythm were "real".

• I highlight the 2 deflections I chose for setting my calipers to the P-P interval that I suspected (using RED arrows in ECG #1).
• In similar fashion as Dr. Frick — I then highlighted (using PINK arrows in Figure-1) periodic signs of additional atrial activity.
• Final "proof" of true AV dissociation was forthcoming when I was able to add (using YELLOW arrows placed at a similar P-P interval) markers in places where it was obvious that underlying regular atrial activity could easily be hidden.

Figure-1: I've labeled the initial ECG and the repeat 12-lead ECG in today's case.

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The Post-Conversion Tracing:

I found several features of the repeat ECG (after spontaneous conversion of the VT rhythm) to be especially interesting.

• We now see regular narrow QRS complexes in ECG #2 — that are conducted with a constant and normal PR interval at the same atrial rate, and with the same P wave morphology as was present in ECG #1 (RED arrows in the long lead V1 rhythm strip in ECG #2). This adds further confirmation that we truly were seeing AV dissociation in ECG #1.
• I suspect that this underlying atrial rhythm is not sinus — because no clearly upright P wave is seen in simultaneously-recorded lead II in the post-conversion tracing (dotted BLUE line showing this P wave's appearance in lead II of the post-conversion tracing). Instead — it looks like underlying atrial activity in both tracings of Figure-1 is from a low atrial rhythm. The low amplitude of these ectopic atrial P waves is another reason why AV dissociation is so subtle in today's case.
• Finally — Dr. Frick details how today's patient was found to have severe, stable coronary disease without evidence of an acute event. However, when I first saw ECG #2 — I had a different impression. Instead, in the setting of large inferior lead Q waves — my "eye" was attracted by: i) A small-but-real amount of inferior lead ST elevation (at least in leads II and III) — with suggestion of reperfusion T wave inversion in lead aVF; — ii) Potentially recent reciprocal change (subtle abnormal ST segment flattening in lead aVL); — and, iii) Potential posterior lead reperfusion T waves in the form of increased T wave positivity in leads V1,V2,V3. I therefore suspected that the cause of this patient's VT may have been recent infero-postero OMI, now with evidence of reperfusion T waves.
• NOTE: Tachycardia is still present in this post-conversion tracing ( = ECG #2). It is important to appreciate that at times — tachycardia may accentuate ST-T wave changes (ST elevation and/or depression) that are no longer present when the heart rate slows. As a result — I recognized that additional follow-up would be needed to determine the significance (if any) of these ST-T wave findings I describe in ECG #2 (and as per Dr. Frick — subsequent evaluation did confirm that none of these changes were acute).