ECG Blog #128 — VT, Fusion, WCT, Sinus Tach

How would you interpret the lead II rhythm strip shown in Figure-1?

• How certain are you of your diagnosis?
• Are the P waves preceding beats #6 and #7 conducting?
• Challenge Question: How many different-shaped beats are there on this tracing?

Figure-1: Long lead II rhythm strip showing a changing rhythm. Can you explain what is happening? 

Interpretation: This is a challenging case. The easiest way to approach the interpretation of more difficult arrhythmias such as this one, is to begin with that part of the tracing that is easiest to interpret. 

• To do this — Mentally block out the first 7 beats on this tracing. If ALL you had to worry about was the last 6 beats in Figure-1 (ie, beats #8-thru-13) — How would you interpret the rhythm in Figure-2?

Figure-2: The first 7 beats from Figure-1 have been blocked out. How would you interpret the arrhythmia represented by beats #8-thru-13?

Answer to Figure-2:

Beats #8-thru-13 are regular at a rate of 110 beats/minute. The QRS complex is narrow, and each QRS is preceded by normal appearing (upright) P waves with a normal PR interval. Beats #8-thru-13 represent Sinus Tachycardia.

• Now mentally block out the last 8 beats on this tracing. If all you had to worry about were the initial 5 beats — How would you interpret the arrhythmia in Figure-3?

Figure-3: The last 8 beats (#6-thru-13) from Figure-1 have been blocked out. How would you interpret the arrhythmia represented by beats #1-thru-5?

Answer to Figure-3:

Beats #1-thru-5 are regular at a rate of just over 100 beats/minute (the R-R interval is just under 3 large boxes in duration). The QRS complex of these beats is wide, bizarre, and not preceded by atrial activity. This suggests a ventricular etiology. Since the usual rate of an idioventricular escape rhythm is much slower (in the range of 30-40 beats/minute) — We describe the arrhythmia represented by beats #1-thru-5 in Figure-3 as an Accelerated IdioVentricular Rhythm ( = AIVR).

• Return to Figure-1. Now focus on the more difficult part of the tracing = beats #5-thru-8. Can you figure out what is going on in Figure-4?
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Figure-4: Beats #1-thru-4 and #9-thru-13 from Figure-1 have been blocked out. Can you figure out what is happening with the remaining beats #5-to-8?

HINT to Figure-4: Sequential consideration of the following 4 questions may lead you to the diagnosis:

• What kind of beat is beat #8? (See Answer to Figure-2).
• What kind of beat is beat #5? (See Answer to Figure-3).
• Would you expect the P wave preceding beat #6 to be able to conduct normally? If not — Why not?
• Think of beats #5 and #8 as “parent beats”. If these parent beats (#5 and #8) were to mate (ie, combine) and “have children” — What would you expect the children to look like?

Answer to Figure-4:

Since the rhythm in Figure-2 is sinus tachycardia, beat #8 must be a sinus-conducted beat. Similarly, since the rhythm represented by Figure-3 is AIVR — beat #5 must be a ventricular beat.

• Note that the PR interval preceding beat #6 is shorter than the PR interval preceding other sinus-conducted beats (beats #8-thru-13 in Figure-1). It is too short to conduct normally.
• Note also that although the QRS complex of beat #6 is entirely upright — it is not nearly as wide as the other upright (ventricular) beats (beats #1-thru-5 in Figure-1). Beat #6 is a Fusion Beat.

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FUSION BEATS

Fusion beats occur as a result of simultaneous occurrence of supraventricular and ventricular impulses. This concept is illustrated in Figure-5.

• Panel A in Figure-5 — schematically shows the pathway of normal conduction (SA Node–to–AV Node – to bundle branches). This results in a sinus-conducted beat (S) with a normal PR interval and a narrow QRS complex.
• In contrast, Panel B — begins in the ventricles (V). This results in a wide QRS complex without preceding atrial activity.
• The phenomenon of Fusion is represented in Panel C — in which there is simultaneous (or near simultaneous) occurrence of a supraventricular and ventricular complex. Depolarization wavefronts meet before they are able to complete their path, and the ECG appearance of the resultant fusion beat takes on characteristics of both the supraventricular and ventricular complex (F).

Figure-5: Illustration of the concept of fusion beats. Panel A — Sinus-conducted beat (S). Panel B — Ventricular beat (V). Panel C — Fusion beats (F1 and F2).

NOTE: Depending on whether the wavefronts in Panel C of Figure-5 meet high or low in the ventricles — the fusion beat will take on more characteristics of either the supraventricular complex (F2 in Panel C) — or, of the ventricular complex (F1 in Panel C).

• Clinically — the reason recognition of fusion beats is important, is that it proves anomalous complexes in a tracing must be of ventricular etiology!

SUMMARY: Now look at Figure-6 — in which we have labeled Figure-1 with RED arrows to indicate the series of regularly-occurring sinus P waves which are clearly seen to begin just before beat #6.

• Close inspection just before widened beat #5 reveals a subtle-but-definite small hump at the onset of the R wave of this beat. This small hump is almost certainly one more P wave (BLUE arrow) — that occurs right on time (ie, at the appropriate P-P interval distance just before the last RED arrow). No sinus P waves are seen before this blue arrow ...

Figure-6: Long lead II rhythm strip taken from Figure-1. We have labeled the regularly-occurring sinus P waves that are clearly seen with RED arrows. The BLUE arrow indicates yet one more on-time P wave that deforms the initial part of beat #5.

From Figure-6 — It should now be apparent that the arrhythmia begins with a 5-beat run of AIVR (at ~100-105/minute). Sinus tachycardia at a slightly faster rate (~110/minute) then takes over (beats #8-thru-13). Beats #6 and #7 manifest a QRS morphology intermediate between that of the ventricular and supraventricular beats, with the former beat (#6) more closely resembling the morphology of ventricular beats (as was the case for F1 in Panel C of Figure-5) — and the latter ( = beat #7) most closely resembling the morphology of the QRS complex during sinus tachycardia (as was the case for F2 in Figure-5).

• The appearance of beats #6 and #7 in Figure-6 is as might be anticipated considering the PR interval that precedes each of these fusion beats. That is, the very short PR interval preceding beat #6 would not be expected to allow sufficient time for deep penetration of the supraventricular impulse (P wave) into the ventricles. Thus, beat #6 much more closely resembles the beats of ventricular etiology.
• In contrast — the PR interval preceding beat #7 is almost normal. As a result, this supraventricular impulse (P wave) should have had time to travel relatively far down the conduction system before fusion occurred (explaining why the beat more closely resembles the morphology of supraventricular beats).
• KEY POINT — Clinically, recognition that beats #6 and #7 in this tracing are fusion beats confirms the ventricular etiology of beats #1-thru-5.

CHALLENGE Question — Return a final time to Figure-6. In addition to beats #6 and #7 — there are 3 more fusion beats in this tracing. Can you spot them?

• PEARL — One looks for fusion beats not only by examining the QRS complex — but also by close inspection of each T wave!

ANSWER to Challenge Question:  Beats #5, #8 and #9 are all fusion beats! The KEY to recognizing fusion beats is to look for the ever-so-slight subtle differences that may be present in either the QRS complex and/or the T wave between the beat(s) in the question and the complexes of known etiology.

• Careful inspection of beat #5 reveals that its R wave is not quite as tall and its T wave not quite as deep as the other ventricular beats. Note also that the very initial portion of the upstroke of this R wave is deformed. A P wave is hiding here — and accounts for the slight degree of fusion that this beat manifests (BLUE arrow in Figure-6).
• Beats #8 and #9 are also fusion beats. Careful comparison of these beats with beats #10-thru-13 reveals that they have a slightly narrower QRS complex and, a T wave that is smaller and less peaked.

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NOTE: For more on Fusion Beats — See our ECG Blog #129 —

ECG Blog #127 (Acute STEMI – Lead Malposition – LVH – Reciprocal Changes)

This 12-lead ECG was obtained from a 61-year old man who was seen by EMS for new-onset chest discomfort. How would you interpret this ECG? Should you call to activate the cath lab en route to the hospital?

Figure-1: 12-lead ECG obtained from a 61-year old man with new-onset chest discomfort. Would you activate the cath lab for suspected acute anterior STEMI? 

Interpretation: There are a number of findings on this ECG that make it difficult not to immediately activate the cath lab. We note the following:

The rhythm is sinus. Intervals are normal. The axis is slightly leftward (at about -15 degrees). Voltage for LVH is satisfied by an R wave in lead aVL that clearly exceeds 12mm in amplitude.

• There is a Q wave in lead V1, a QS in V2 — and no more than the tiniest of r waves in lead V3. Thus, R wave amplitude is clearly reduced in the anterior leads — and Q waves in V1,V2 could be consistent with septal infarction.
• The T wave in leads V2-thru-V5 looks like it may be hyperacute. T wave amplitude in lead V2 seems disproportionately tall compared to the QRS complex in this lead. In addition, the amount of J-point elevation in leads V4 and V5 seems more-than-is-normally-expected in these leads, especially given relatively small R waves in V4,V5.
• There is ST elevation in lead aVL that looks to be the mirror-image of lead III.
• There appears to be reciprocal change in the inferior leads (more subtle in lead II, since there is only some ST-T flattening in this lead …).

Considering the above findings together — one needs to be concerned about the possibility of acute LAD occlusion in this 61-year old man with new-onset symptoms. That said, there are a number of features against this being an acute anterior STEMI. These include:

• Probable Lead Malposition — It is surprising how frequently leads V1 and V2 are placed too high on the chest. Doing so may give false impression of anterior infarction. Clues that precordial leads have probably been placed one (or even two) interspaces too high include: i) a significant negative component to the P wave in lead V1 and/or V2; and, ii) the finding of an r’ deflection in either V1 and/or V2. Both of these findings are present in Figure-1. Perhaps lead V3 is then also malpositioned? So maybe there is not loss of r wave (and development of Q waves) after all in the anterior leads?
• The mean QRS Axis is Leftward. This might account for normal T wave inversion in predominantly negative limb leads III and aVF.
• Early Repolarization in Leads I, aVL? — Shape of the J-point ST elevation in these lateral leads is concave-up (ie, “smiley”-configuration) with small, narrow septal q waves and J-point notching. This has the appearance of early repolarization.
• There is LVH. As mentioned, voltage criteria for LVH are clearly met in lead aVL (that easily surpasses an R wave amplitude of ≥12mm). What about R wave amplitude in lead V6? Close vertical placement of lateral chest leads with resultant overlap makes it very difficult to discern just how tall the R wave in lead V6 is, but I suspect it surpasses 18mm once one mentally “subtracts” the overlap. LVH is notorious for producing a reciprocal “strain” pattern in anterior leads — and this could account for at least some of the suspicious T wave appearance in leads V2,V3.

BOTTOM LINE — If the history in this case was worrisome, then this patient most likely needs timely cardiac catheterization. One has to be able to rule out acute stemi with more certainty than I have from looking at this single tracing. But my thought on seeing this ECG was that I would not be surprised if cath turned out to be unremarkable.

• That said, there DOES seem to be more ST elevation-than-I-would-expect given QRS appearance in leads V4,V5 — so I would also not be surprised if cath showed acute LAD occlusion.
• It is FINE not to be certain from review of a single tracing as to whether or not acute infarction is occurring. Depending on clinical circumstances — one might either decide to repeat the ECG and obtain stat Echo (looking for wall motion abnormality) in the Emergency Department — or, simply proceed to cath for definitive diagnosis.
• Follow-Up — This patient did not have acute infarction ...

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Acknowledgment: — My thanks to Dustin Carter and James Criscitiello (from New York, New York) for their permission to use this case and ECG.

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