I was sent the ECG shown in Figure-1 — told that the patient was a previously healthy 30-ish year old man who was seen by paramedics in the field for nausea and vomiting, which a little bit later was followed by CP (Chest Pain).
- NOTE: This tracing does not satisfy STEMI criteria (ie, Sufficient ST elevation in at least 2 contiguous leads is lacking — which to qualify as a STEMI, would require ≥2 mm for leads V2,V3 in men and/or ≥1 mm for other leads).
QUESTION:
- Despite not satisfying STEMI criteria — Were the paramedics correct to request activating the cath lab given ECG #1?
Figure-1: The initial ECG in today’s case. |
MY Thoughts on the ECG in Figure-1:
In a patient with new CP — ECG #1 is a worrisome tracing. The rhythm is sinus tachycardia at ~100/minute — with normal intervals, normal axis, and no chamber enlargement. I’ve highlighted the worrisome ECG findings in Figure-2:
- My “eye” was immediately captured by the 3 leads within the RED rectangle. As highlighted by the RED arrows — the T waves in leads V1,V2,V3 are all peaked and disproportionately taller-than-they-should-be in these anterior leads (in comparison with modest size of each QRS complex).
- Normally the T wave in lead V1 is either negative, or no more than minimally positive without noticeable ST elevation (which is very different than what we see in Figure-2).
- The hyperacute T waves in leads V2 and V3 — dwarf the QRS in these leads, with there being inappropriate (albeit <2 mm) ST elevation in lead V2. Ignoring the 3rd QRST complex in lead V3 (that is distorted by artifact) — the ST segment in lead V3 is inappropriately flat, if not slightly depressed.
- In the context of obviously hyperacute T waves in leads V1,V2,V3 — neighboring chest leads V4,V5 also manifest taller and more-peaked-than-they-should-be T waves that are hyperacute (BLUE arrows in these leads).
In addition — the limb leads in Figure-2 are abnormal:
- As is so often the case with acute proximal LAD OMI — lead aVL manifests ST elevation (RED arrow in this lead).
- Reciprocal ST depression is seen in each of the inferior leads (BLUE arrows in leads II,III,aVF).
IMPRESSION: Regardless of whether or not the “millimeter-definition” for a STEMI is satisfied — in this patient with new CP — this initial ECG in today's case is diagnostic of acute proximal LAD OMI.
- The cath lab should be immediately activated.
Figure-2: I've labeled the initial ECG in today's case. |
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30 Seconds Later ...
- In Figure-3 — What do we now see in lead V3 in this repeat ECG, done just 30 seconds later?
Figure-3: Comparison between ECG #1 — and the repeat ECG done just 30 seconds later. What do we now see in lead V3? |
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ANSWER:
- In Figure-3 — there is now T-QRS-D (Terminal QRS Distortion) — which is defined as the absence of both a J-wave and an S-wave in either lead V2, lead V3, and/or lead V4 (as discussed in ECG Blog #318).
- The clinical significance of T-QRS-D — is that it is virtually diagnostic of acute OMI (ie, of acute coronary Occlusion).
- In Figure-4 — Compare the QRST complex in lead V3 for both ECG #1 and ECG #2. Ignoring the 3rd QRS in lead V3 of ECG #1 (which is distorted by artifact) — Note that the S wave has been "lifted" above the baseline in ECG #2, which qualifies as T-QRS-D.
- To Emphasize: Clearly, T-QRS-D is not needed in today's case to make the diagnosis of acute LAD OMI — since multiple findings described above more than suffice to justify immediate cath lab activation. But there are occasions in which ST-T wave findings may be far more subtle, for which recognition of T-QRS-D may prove to be the decisive diagnostic feature.
- Additional NOTE: 3 ECG findings combine to suggest a proximal location for today’s acute LAD occlusion. These are i) Hyperacute T waves in the chest leads that begin in lead V1; — ii) ST elevation is seen in lead aVL; — and, iii) There is reciprocal ST depression in all 3 inferior leads.
Figure-4: T-QRS-D is now seen in ECG #2. |
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4 Minutes after ECG #2 ...
- What do we now see in Figure-5 — which compares the next serial tracing that was recorded 4 minutes after ECG #2?
Figure-5: Comparison between ECG #2 — and the next tracing recorded 4 minutes later. Has there been much change? |
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ANSWER:
In just 4 minutes — there have been a number of dynamic ST-T wave changes that we now see in Figure-5. These changes are best appreciated by lead-to-lead comparison, and include the following:
- The most remarkable ST-T wave changes have been in the chest leads — which now show obvious ST elevation (most marked in leads V2,V3 — but also in neighboring leads V1 and V4).
- Note further “lifting” of the J-point in lead V3 — resulting in more pronounced T-QRS-D compared to ECG #2.
- ST-T wave changes in ECG #3 (compared to ECG #2) are more subtle in the limb leads — but clearly show a more acute appearance to the inferior lead reciprocal depression and to the hyperacute T wave in lead aVL.
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2 Minutes after ECG #3 ...
- What do we now see in Figure-6 — which compares the next tracing ( = ECG #4) recorded 2 minutes after ECG #3?
Figure-6: Comparison between the chest leads from ECG #3 — and the next 12-lead ECG, that was recorded 2 minutes later. What do we now see? |
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ANSWER:
In Figure-6 — We now see a run of ventricular beats.
- The first 3 beats in the limb leads from ECG #4 are sinus-conducted (with the RED arrow in lead II highlighting that there are upright sinus P waves with a constant and normal PR interval in this lead). Of note in ECG #4 — although the QRS complex “looks” wide in a number of leads for sinus-conducted beats — the QRS does not measure more than 0.10 second for these sinus-conducted beats (therefore not qualifying as wide).
- Beginning with beat #4 in the limb leads of ECG #4, and continuing through to beat #8 — P waves are lost and the QRS widens, with a constantly changing QRS morphology. I interpreted beats #4-thru-8 as a 5-beat run of PMVT (PolyMorphic Ventricular Tachycardia) — which presumably was precipitated by acute ischemia from the ongoing extensive MI.
- Ironically — there is less ST elevation in the chest leads of ECG #4 compared to ECG #3 — despite the fact that we now see a run of PMVT.
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CASE Follow-Up:
Shortly after ECG #4 was obtained — the patient developed VFib. Prolonged resuscitation, including numerous defibrillation attempts failed to convert the patient to a sustainable sinus rhythm. Unfortunately — the patient could not be resuscitated, as persistent VFib ultimately deteriorated to asystole.
- Presumably the patient died of cardiogenic shock from extensive anterior infarction.
Ischemic PMVT with Acute MI:
- Recent decades have seen a dramatic decrease in the incidence of sustained VT deteriorating to VFib as the ultimate lethal event in patients with acute MI. Prompt treatment with reperfusion of the "culprit" artery is largely responsible for the improved prognosis with these patients.
- That said — despite prompt treatment by paramedics on the scene in today's case — refractory VFib developed, and the patient could not be resuscitated.
- Clues to this patient's ultimate demise include: i) Extensive myocardial damage from acute proximal LAD occlusion (presumably resulting in cardiogenic shock with asystole as the terminal rhythm); — and ii) The run of PMVT seen in Figure-4 — with occurrence of this arrhythmia in the setting of acute infarction portending an extremely poor prognosis (Bhar-Amato — Arrhythmia Electrophysio Rev 6(3): 134-139, 2017 — and — Viskin S et al — Circulation 144(10): 823-839, 2021).
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Acknowledgment: My appreciation to Konstantin Тихонов (from Moscow, Russia) 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.
- ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = an acute coronary Occlusion MI).
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- CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
- CLICK HERE — for my 2 new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).
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- Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
- Recognizing ECG signs of Precordial Swirl (from acute OMI of LAD Septal Perforators) — See My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog.
- ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
- ECG Blog #230 — Reviews how to compare serial ECGs.
- ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
- ECG Blog #268 — Shows an example of reperfusion T waves.
- ECG Blog #400 — Reviews the concept of "dynamic" ST-T wave changes.
- ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).
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