ECG Blog #334 — What do the 12 Leads Show?

The ECG in Figure-1 — was obtained from an older woman. Unfortunately — No other clinical information was available.

• How would YOU interpret this ECG?

Figure-1: 12-lead ECG obtained from an older woman. No clinical history was available.

MY Thoughts on the ECG in Figure-1:

Many readers of this blog encounter the same situation that I often find myself in — namely, having to interpret tracings without the benefit of any clinical history. That was the case for me with today's tracing. (I initially did not even have the benefit of a long lead rhythm strip).

• The rhythm in Figure-1 (for the 11 beats that we see on this tracing) — appears to be fairly regular at a rate just under 70/minute.
• The QRS complex is narrow everywhere.
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• P waves are absent in lead II!

QUESTION:

• What is the rhythm in ECG #1?

ANSWER:

• See Figure-2 ... 

Figure-2: I've labeled atrial activity from Figure-1 (which is confirmed by provision of a long lead rhythm strip).

Continuing My Interpretation of Today's Tracing:

The fact that there is no upright P wave in lead II in Figure-1 — tells us that the rhythm is not sinus!

• PEARL #1: Although lead II is clearly the most helpful of the 12 leads on a standard ECG for determining the cardiac rhythm — this lead will not always show atrial activity. When no clearly upright P wave is seen in lead II — then: i) The rhythm is not sinus (assuming there is neither dextrocardia nor lead reversal); and, ii) We need to focus on the remaining 11 leads in our search for atrial activity. Of these remaining 11 leads — I have found lead V1 to be 2nd-best for detecting atrial activity — followed by leads III, aVR, aVF, and/or lead V2 — followed by taking a close look at the 6 leads that remain.

The Rhythm is Revealed in Figure-2:

The 12-lead ECG in today's case provides an excellent example of how lead V1 may sometimes reveal atrial activity not evident in any of the other 11 leads. RED arrows in Figure-2 suggest there is 2:1 AV conduction for the 3 beats that occur in lead V1!

• The long lead rhythm strip at the bottom of Figure-2 (with simultaneously-recorded leads V1 and II) — confirms 2:1 atrial activity throughout!
• Note that the PR interval before each of the 11 beats on the long lead rhythm strip is constant — which confirms that 1 out of every 2 P waves are conducted to the ventricles.
• The RHYTHM: Since the ventricular rate is just under 70/minute — this means that the atrial rate = 2X this, or ~135-140/minute. Since this atrial rate is well below the atrial rate usually seen with AFlutter — and since the baseline between P waves is flat (ie, there is no "sawtooth" pattern) — the rhythm in ECG #1 = ATach (Atrial Tachycardia) with 2:1 Block.

Continuing Interpretation of the Rest of the 12-Lead:

Now that we've interpreted the rhythm in Figure-2 — we can complete interpretation of the rest of this tracing:

• Intervals (PR - QRS - QTc): We've already established that the QRS complex is narrow in all 12 leads. The PR interval looks to be a little long (ie, >0.20 second) — although the non-sinus origin of atrial activity may account for this. The QTc does not appear prolonged (ie, clearly less than half the R-R interval).
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• Axis: The frontal plane axis is normal (ie, about +40 degrees).
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• Chamber Enlargement — There is probable LVH (ie, the deepest S wave is in lead V2 [ =19 mm] + the tallest R wave, which is in lead V5 [ =18 mm] is ≥35 mm).

Regarding Q-R-S-T Changes:

• Q waves: There is a QS complex in lead V1 (though by itself — this is not abnormal — and a small-but-definitely-present initial r wave is present in lead V2).
• R Wave Progression — is normal (with Transition occurring between lead V3-to-V4).
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• ST-T Wave Changes: There is slight J-point ST depression in a number of leads (most marked in leads V4,V5,V6) — with T wave inversion in at least 9/12 leads (most marked in leads V3,V4,V5).
• There is slight ST elevation in lead aVR.
• The most "eye-catching" lead — is lead V3, which shows a straightened (almost coved) ST segment takeoff that terminates in a deep and symmetrically inverted T wave.
• The T wave in lead V2 appears to be biphasic (ie, positive-negative) — with rapid descent from the initially positive portion of the T wave.

Putting It All Together:

Fully aware that we lack clinical information — My Thoughts on today's tracing were as follows:

• There is an abnormal rhythm = ATach with 2:1 AV Block (with an atrial rate of ~135-140/minute).
• Voltage criteria for LVH are satisfied.
• J-point ST depression is seen in multiple leads — with symmetric T wave inversion (that is quite deep in leads V3,V4,V5) — with an ST-T wave shape that resembles a Wellens'-type morphology.
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• PEARL #2: Although the shape of the ST-T wave depression that we see in lateral leads I, aVL and V5,V6 is consistent with LV "strain" (in association with LVH voltage criteria) — ST-T wave changes of "strain" do not normally extend as far over as lead V3 (and should certainly not be maximal in mid-precordial leads V3,V4 when this is solely the result of LVH). So, while a component of the ST-T wave changes we see in today's tracing may reflect LVH — the Overall Picture (ie, with ST depression and T wave inversion in at least 9/12 leads) clearly suggests ischemia (which depending on the history, could be recent or acute).
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• PEARL #3: While the shape of the ST-T wave in leads V2 and V3 is consistent with what may be seen with Wellens' Syndrome — this diagnosis can not be made without a history of previous chest pain that has now resolved at the time the ECG being looked at is recorded (See ECG Blog 254).
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• PEARL #4: A number of conditions may result in similar ST-T wave changes as are seen in Figure-2. These include: i) Diffuse cardiac ischemia (given ST-T wave changes in 10/12 leads!); ii) Wellens' Syndrome (IF the history is consistent) from a tight, proximal LAD (Left Anterior Descending) stenosis; iii) Recent infarction — in which there are now ST-T wave changes from reperfusion of the "culprit" artery (See ECG Blog #294); iv) Hypertrophic cardiomyopathy (See ECG Blog 309); v) Myocarditis — or other underlying cardiac problem; vi) A "memory" effect from sustained arrhythmia (if the ATach has been present for an extended period of time); and/or, vii) Some combination of the above factors!
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• BOTTOM Line: There are multiple possible reasons that may account for the ECG findings described above. The task falls on us to correlate this tracing with the clinical situation to determine IF an acute cardiac process is ongoing.

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ADDENDUM (9/24/2022): In the following 2 Figures — I post written summary from my ECG-2014-ePub regarding Wellens’ Syndrome. 

• CLICK HERE — for a PDF of this 3-page file on Wellens’ Syndrome that appears in Figure-3 and Figure-4.

 

 

Figure-3: Regarding Wellens’ Syndrome (from my ECG-2014-ePub).

Figure-4: Wellens’ Syndrome (Continued). 

—  — 

ECG Media PEARL #26a (7:40 minutes Audio) — Reviews what Wellens' Syndrome is — and what it is not (from ECG Blog #254).

 

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).  
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• ECG Blog #209 — Reviews a case of marked LVH that results in similar ST-T wave changes as may be seen with Wellens' Syndrome.
• ECG Blog #254 — Reviews what Wellens' Syndrome is and is not.
• ECG Blog #309 — Reviews distinction between LVH, Wellens' Syndrome — vs — HCM (Hypertrophic CardioMyopathy).
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• See My Comment at the bottom of the page in the August 12, 2022 post in Dr. Smith's ECG Blog — for review on the History of Wellens' Syndrome (with reference to the original 1982 article by Zwaan, Bär & Wellens).
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• ECG Blog #245 — Reviews my approach to the ECG diagnosis of LVH (outlined in Figures-3 and -4, and the subect of Audio Pearl MP-59 in Blog #245).
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• ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused (with Audio Pearl MP-11 in Blog #294).