ECG Blog #319 — QRS Alternans?

The ECG in Figure-1 — was obtained from a 59-year old man who presented to the ED (Emergency Department) with new-onset chest pain.

• How would YOU interpret the ECG in Figure-1?
• Why is QRS morphology changing?
• Should you activate the cath lab?

Figure-1: The initial ECG in the ED.

MY Thoughts on the ECG in Figure-1:

The underlying rhythm appears to be sinus — at a rate just under 100/minute. Of note is the observation that QRS morphology changes every-other-beat. This alternating QRS morphology is more apparent in some leads compared to others.

• Despite the changing QRS morphology — sinus P waves remain precisely regular throughout this tracing (RED arrows in the long lead II rhythm strip in Figure-2).
• What is different — is that every-other-beat, the PR interval shortens and we see delta waves that prolong the QRS. Delta waves are both positive and negative — and they are present in virtually all leads (BLUE arrows).
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• BOTTOM Line: The rhythm in Figure-2 is sinus at a rate just under 100/minute. The patient has WPW (Wolff-Parkinson-White) Syndrome — and every-other-beat is conducted with preexcitation!

PEARL #1: The 2 entities to consider in the differential diagnosis of the rhythm in Figure-2 are: i) Ventricular bigeminy with late-cycle PVCs; and, ii) Electrical alternans. 

• Precise regularity of sinus P waves in the long lead II rhythm strip (RED arrows) — with the identical distance from the onset of P waves until the end of the QRS tells us that the odd-numbered beats do not occur early (ie, that odd-numbered beats are not PVCs).
• Rather than true electrical alternans — the rhythm in Figure-2 is a form of "pseudo-alternans". True electrical alternans would not develop delta waves (and would be unlikely to manifest as dramatic a change in QRST morphology as is seen in a number of leads).

Figure-2: I've labeled P waves (RED arrows) — and delta waves (BLUE arrows) from the initial ECG (See text).

Assessment of ST-T Wave Changes in ECG #1:

In my experience — it is rare that we are able to identify acute infarction in a patient with WPW. It is possible to see acute ST-T wave changes during preexcitation (See ECG Blog #157) — but most of the time in patients with WPW, acute ST-T wave changes of infarction will be hidden within the QRST complex.

• Today's case is unique — in that it provides us with an insightful opportunity to assess the effect that preexcitation may have in a patient with acute infarction.

Even-numbered beats in Figure-2 are conducted normally:

• Focusing attention on simultaneously-recorded beats #2,4,6 and 8 in the limb leads — We see relatively low-voltage, narrow QRS complexes with left axis deviation consistent with LAHB (predominant negativity for the QRS  of beats #2 and 4 in lead II).
• There is T wave inversion in leads III and aVF (ie, for beats #2,4; and 6,8).
• There appears to be ST segment flattening, and perhaps a hyperacute T wave in lead I (for beats #2,4).
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• In the chest leads — There is a QS complex in leads V1,V2 — with no more than a tiny positive r wave in lead V3 (for beats #10,12). Transition never occurs — as the R wave in lateral chest lead V6 remains smaller than the S wave in this lead (for beats #14,16).
• The most remarkable finding in the chest leads — is the 2-3 mm of J-point ST elevation in leads V1,V2,V3 (for beats #10,12) — with an abnormally straightened ST segment takeoff in lead V1 — and disproportionately tall and peaked T waves in leads V2,V3.
• Disproportionately tall and peaked (hyperacute) T waves continue in leads V4 and V5 (for beats #14,16).
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• IMPRESSION: Given the history of new-onset chest pain — I interpreted the chest lead ST-T wave changes as consistent with deWinter-like T waves — if not frankly consistent with recent or acute LAD (Left Anterior Descending) coronary artery occlusion. 
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• PEARL #2: As discussed in ECG Blog #183 — Typical deWinter T waves manifest 1-3 mm of upsloping J-point ST depression in at least a few leads, prior to continuing into tall, peaked T waves. I favor the term, "deWinter-like" T-waves when this J-point ST depression is lacking (as it is in ECG #1) — since the concept (ie, LAD occlusion) is the same, with the probable reason ST depression is missing being dependent on the timing of the ECG with respect to evolution of the process.
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• PEARL #3: ECG findings in favor of a more proximal location of LAD occlusion include: i) Onset of ST elevation as soon as lead V1; ii) Maximal T wave peaking in leads V2,V3; iii) Hyperacute lateral limb lead changes (ie, Considering modest QRS amplitude — I interpreted the T waves of beats #2,4 in lead I and the T wave of beats #6,8 as hypervoluminous); and, iv) Reciprocal ST-T wave changes in the inferior leads (especially in leads III and aVF).
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• PEARL #4: Did you notice slurring in the initial downslope of the QS complex in lead V2? This subtle-but-real fragmentation of the initial QS downslope suggests "scar" — which in the context of the ST-T wave changes seen in ECG #1, suggests anterior infarction has already taken place.

Returning to interpretation of ST-T wave changes in ECG #1 — the odd-numbered beats in Figure-2 show preexcitation:

• Most of the preexcited beats show nonspecific ST-T wave changes that are not indicative of recent infarction. The exceptions are beats #9 and 11 in leads V1 and V2 — both of which manifest marked (and unexpected) ST elevation. The shape of the ST-T wave for preexcited beats #9 and 11 in lead V1 clearly looks different than what one would expect with simple preexcitation.

The CASE Continues:

A prior ECG (recorded 3 years earlier) was found (Figure-3).

• Compare QRS and ST-T wave morphology of the preexcited beats in ECG #1 — with the baseline ECG #2 (that was recorded 3 years earlier).
• In retrospect (ie, with the benefit of this baseline tracing) — which leads in ECG #1 showed acute ST-T wave changes in those beats that conducted with preexcitation?

Figure-3: Comparison of the initial ECG — with a baseline ECG obtained 3 years earlier. What differences do you see?

Comparison with the Prior ECG:

The prior ECG recorded 3 years earlier ( = ECG #2 in Figure-3) — showed preexcitation of every beat! This confirmed our presumption that this patient has WPW.

• The most striking difference in ST-T wave morphology between preexcited beats in ECG #1 — and preexcitation in ECG #2 — was in leads V1 and V2. The fact that there was no ST elevation at all in these leads in the baseline tracing confirms that the J-point ST elevation seen in beats #9 and 11 of ECG #1 was acute!
• In addition — Note that the very tall, peaked T waves seen for preexcited beats in leads V2-thru-V5 of ECG #1 were not present in the baseline ECG. This confirms that deWinter-like T waves were indeed manifest in the preexcited beats of ECG #1.

CASE Follow-Up:

Troponin came back markedly elevated. Cardiac cath was performed — and revealed single-vessel disease in the form of a high-grade proximal LAD stenosis, consistent with recent infarction.

• Take-Home Point: Although most of the time you will not be able to recognize acute infarction when there is preexcitation — On occasion, ST-T wave changes may be so abnormal as to allow this diagnosis. Such was the case for preexcited beats in leads V1 and V2 of ECG #1.

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #83 — Reviews the concept of Electrical Alternans.
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• ECG Blog #153 — What IF WPW is incidentally discovered?
• ECG Blog #121 — WPW with intermittent Delta Waves (ie, the Concertina Effect).
• ECG Blog #157 — Reviews a case of WPW that simulates acute MI.
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• ECG Blog #183 — Reviews the concept of deWinter-like T waves.