ECG Blog #340 — An Evolution to Make Note Of

The ECG shown in Figure-1 was recorded in a primary care clinic — from a patient who presented with new-onset chest pain.

• How would YOU interpret the ECG shown in Figure-1?
• Is this hyperkalemia? — or is there a “culprit” artery?

Figure-1: The initial ECG in today’s case — recorded in a primary care clinic from a patient who presented with new-onset chest pain.

MY Thoughts on ECG #1:

Although I would clearly verify with a blood draw that serum K+ is normal — I strongly doubt that the tracing shown in Figure-1 represents hyperkalemia because:

• This patient presented to an out-patient clinic with a history of new-onset chest pain. This is an unlikely presentation for acute hyperkalemia.
• Although T waves are tall and peaked (pointed) with a narrow base in a number of chest leads — there is dramatic J-point ST depression in each of these leads (which is not an expected finding of hyperkalemia).
• The ECG appearance in the 6 limb leads does not look at all like hyperkalemia.

Instead — the history and ECG picture in Figure-1 is highly suggestive of ACS (Acute Coronary Syndrome) — most likely with acute OMI (Occlusion-based Myocardial Infarction). I see the following:

• The rhythm is sinus at ~70/minute. All intervals (PR, QRS, QTc) and the frontal plane axis are normal. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q Waves: Each of the 3 inferior leads (II,III,aVF) show fairly large Q waves (especially in leads III and aVF) — when compared to R wave amplitude in those same leads. These Q waves are suggestive of inferior infarction at some point in time (See below). In contrast — the very small and narrow q waves that are seen in lateral chest leads V5 and V6 are most likely “normal septal q waves”.
• R Wave Progression: There is early transition in ECG #1 — with abrupt development (already by lead V2) of an R wave that is at least as tall as the S wave is deep. Thereafter — R wave amplitude continues to appropriately increase, with peak R wave amplitude attained in leads V4,V5.

Regarding ST-T Wave Changes:

The most remarkable ECG abnormalities in ECG #1 relate to ST-T wave changes.

• As noted — T waves are tall and peaked, with a narrow base in at least 4 (if not 5) of the chest leads (ie, in leads V2-thru-V5 — if not also in lead V6).
• Each of the leads with tall, peaked T waves manifest dramatic J-point ST depression (of between 3-to-5 mm in leads V2-thru-V5).
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• NOTE: There is prominent J-point notching in leads V3,V4,V5 (and more subtly in lead V6) — with “eye-catching” downsloping of ST segments in those chest leads with ST depression.
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• In contrast — ST-T wave changes in the limb leads look much less acute. There is a hint of ST segment coving with T wave inversion in lead III — but without ST elevation. Other limb leads show nonspecific ST segment flattening, with some ST depression in leads I and aVL — but not nearly to the same extent as is seen in the chest leads.

Putting It All Together:

As emphasized — Given the history of new-onset chest pain — and — the ECG picture in Figure-1 — We need to assume acute OMI until proven otherwise! Beyond this obvious conclusion — I found a number of interesting features associated with this tracing:

• I did not know what the “culprit” artery was from this initial tracing in Figure-1. The large inferior lead Q waves — with abrupt early transition in the chest leads — strongly suggests infero-postero infarction has occurred at some point in time. But IF myocardial injury in these 2 anatomic areas is all "new" — then the difference in acuity suggested by limb lead vs chest lead ST-T wave findings conveys a discrepancy in timing (since limb lead findings look much less acute compared to far more dramatic ST-T wave findings in the chest leads). 
• Other Possibilities: The infero-postero MI could be old — and the ST-T wave findings in the chest leads could represent an early stage in an acute ongoing form of deWinter T Waves (See ECG Blog #183). Alternatively — ECG #1 could reflect some other pattern of multi-vessel disease.
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• BOTTOM Line: Regardless of what the "culprit" vessel(s) turned out to be — Acute intervention was needed! Ideally — prompt cath would be done to define the anatomy and guide treatment. Alternatively — acute thrombolysis could be initiated.

CASE Follow-Up:

The patient was treated with Streptokinase. For illustrative purposes in Figure-2 — I've consolidated the evolution of QRST changes by focusing on the Chest Leads over the course of 6 serial ECG tracings.

• NOTE: Limb lead tracings over the course of these 6 serial ECGs failed to show any evolution of ST-T wave changes in the inferior leads. The inferior MI was old.

Figure-2: Chest lead tracings from the next 6 serial ECGs obtained on today's patient. Limb lead tracings failed to show evolution of ST-T wave changes in the inferior leads.

Evolution of the Chest Leads over 6 Serial ECGs:

For clarity — Figure-2 compares serial ECG changes in the Chest Leads over the course of 6 tracings. The timing of these 6 tracings is as follows:

• Panel A: T = 0 (ie, These are the Chest Leads taken from the initial ECG in today's case — the complete 12-lead of which is shown in Figure-1).
• Panel B: T = 1 hour (Chest leads from initial ECG that was recorded when the patient arrived in the ED).
• Panel C: T = 2 hours (from the ECG obtained just prior to STK).
• Panel D: T = 2 hours, 45 minutes (Obtained just after STK completed).
• Panel E: T ~ 4 hours (Obtained ~ 1 hour after STK).
• Panel F: T ~ 12 hours (Patient with minimal chest pain).

MY Thoughts on Figure-2:

Unfortunately — I could not obtain chest pain severity scores correlated to each of the tracings shown in Figure-2. Nevertheless — I thought the evolution of QRST changes in the chest leads of these 6 serial tracings to be remarkable and insightful for another variation of deWinter-like T Waves (See ECG Blog #183 and Blog #318 for more on deWinter-like T Waves).

Panel A (T = 0):

• Chest leads in the initial ECG from today's case highlight how dramatic both the J-point ST depression and T wave peaking can be during the very early stages of deWinter T Waves. 
• Rather than a uniquely upsloping ST segment that leads into the very tall deWinter T waves — the ST segment with this entity may initially be downsloping, as it is here.
• Note how prominent the J-point notching is at the onset of the marked ST depression in leads V3,V4,V5 (and to a lesser extent in lead V6). I believe these exaggerated J-point waves are ischemic-induced Osborn waves — that become smaller as this case evolves, eventually disappearing by Panel C (See My Comment at the bottom of the page in the November 22, 2019 post in Dr. Smith's ECG Blog).

Panel B (T = 1 hour):

• Just 1 hour later — this tracing is remarkable for the loss of anterior lead R wave amplitude! J-wave prominence and the amount of ST depression are greatly reduced. Although the absolute height of the tall T waves is not much different than it was in Panel A — considering the greatly reduced R wave amplitudes — these chest lead T waves are fatter-at-their-peak — wider-at-their-base — and now ever so much more disproportionate (hypervoluminous) to the QRS in their respective leads. These are the hyperacute T waves of an evolving deWinter pattern from acute LAD (Left Anterior Descending) occlusion in progress.

Panel C (T = 2 hours):

• Another hour later (just before Streptokinase was started) — there is subtle evidence of further evolution in that: i) Ischemic J-point notching is no longer seen; and, ii) Downsloping ST depression has been replaced by a steeper, rapidly-rising ascending ST segment that peaks into tall T waves. These are typical deWinter T waves.

Panel D (T = 2 hours, 45 minutes):

• This ECG picture immediately after completion of Streptokinase is not encouraging. There is further overall reduction in chest lead R wave amplitude. ST depression is now minimal — but T waves are massive with respect to the R waves in leads V2, V3, V4. Unfortunately — I do not have information correlating the presence and severity of chest pain before, during and immediately after Streptokinase infusion — but it appears that the result of thrombolysis is at best suboptimal.

Panel E (T ~ 4 hours):

• About 1 hour after completion of Streptokinase infusion — definite ST elevation is now apparent in lead V3. That this ST elevation is diffuse and increasing — is evident in the 12-lead ECG shown in Figure-3, that was obtained 30 minutes later (ie, about 90 minutes after completion of Streptokinase).

Panel F (T ~ 12 hours):

• Final evidence of failed thrombolysis is seen in the last set of chest leads — obtained the next day. QS complexes are now seen in leads V1-thru-V4 (in marked contrast to the tall R waves with early transition that were present in Panel A). ST-T waves have returned to baseline — but at no time were "reperfusion T waves" seen. The patient has lost significant myocardium.

The ECG in Figure-3:

I've labeled the 12-lead ECG in Figure-3 as ECG #E2, since this 12-lead tracing was recorded ~30 minutes after the 6 chest leads shown in Panel E of Figure-2 ( = about 90 minutes after completion of Streptokinase).

• Although we lack a continuous long lead rhythm strip — it appears that a bigeminal rhythm is present in Figure-3. 
• Every-other-beat is wide — manifests RBBB/LAHB morphology — and is not preceded by a premature P wave. Therefore — I suspect the rhythm is ventricular bigeminy, with beats #2 and #4 in both limb leads and chest leads being fascicular PVCs arising from the left posterior hemifascicle.
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• Clinical implications of fascicular PVCs are the same as the implications for PVCs arising from ventricular myocardium. Given the clinical context of today's case (ie, extensive LAD occlusion with suboptimal, if not "failed" thrombolysis) — frequent ventricular ectopy suggests ongoing ischemia.
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• Note in ECG #E2 (obtained ~90 minutes after completion of Streptokinase) — that there are anterior Q waves + persistent ST elevation in leads V2-thru-V5 (with marked ST elevation in leads V3,V4).
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• As a didactic point — Note that excessive ST elevation is also present in the fascicular PVCs. PEARL: On occasion — acute MI may be diagnosed by the presence of abnormal ST elevation in PVCs (but not be present in any of the standard 12 leads). As a result — it's good to routinely assess ventricular ectopy for the presence of abnormal ST elevation, especially when standard leads do not yield a definitive diagnosis.
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• BOTTOM Line: Today's case illustrates another variation of deWinter-like T waves — showing ST-T wave evolution over the course of 6 sequential chest lead tracings — with the unfortunate end result of suboptimal (if not completely failed) thrombolysis, with ultimate dramatic loss of R wave amplitude in the final set of chest leads (Panel F in Figure-2).

Figure-3: The 12-lead ECG obtained ~90 minutes after completion of Streptokinase infusion (ie, about 30 minutes after the chest leads shown in Panel E of Figure-2). Ventricular Bigeminy is present in the form of left posterior fascicular PVCs ( = beats #2 and 4 in the limb leads — and beats #2 and 4 in the chest leads). ST-T wave changes are minimal in the limb leads. In contrast — there is marked ST elevation in leads V3 and V4 of the chest leads in both sinus-conducted beats and in the PVCs! (with a lesser amount of ST elevation in neighboring leads).

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Acknowledgment: My appreciation to Eelin Siow and Kianseng Ng (from Malaysia) 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 (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).
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• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "culprit" artery. NOTE: The Audio Pearl reviews the concept of why the term "OMI" ( = Occlusion-based MI) should replace the more familiar term STEMI.  
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• ECG Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data.
• ECG Blog #80 — Reviews determination of the "culprit" artery and application of the Mirror Test for recognition of acute Posterior MI.
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• ECG Blog #248 — Reviews a case that illustrates Causes of a Tall R Wave in Lead V1 (with the Audio Pearl in this post devoted to this subject).
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• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post).
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• ECG Blog #262 — Reviews a case of recent acute Infero-Postero MI with group beating from Wenckebach conduction and Low Voltage (with a list of the causes of Low Voltage).
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• ECG Blog #266 — Reviews some considerations when distinguishing between deWinter T Waves vs Posterior MI.
• ECG Blog #183 — Reviews a case of deWinter T Waves (with the Audio Pearl in this post discussing some variants of the deWinter T wave pattern). 
• ECG Blog #53 — Reviews another case of deWinter T Waves.
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• ECG Blog #318 — Provides another variation of de-Winter-like T waves — and — Reviews (and illustrates) the concept of T-QRS-D (Terminal-QRS-Distortion).
• ECG Blog #215 — Reviews a case with T-QRS-D.
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• ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
• ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?"). 
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• The November 22, 2019 post in Dr. Smith's ECG Blog (Please scroll down to the BOTTOM of the page for My Comment regarding ischemia-induced Osborn Waves).