The ECG in Figure-1 was obtained from a previously healthy older man — who presented to the ED (Emergency Department) with new but atypical CP (Chest Pain) for several hours.
QUESTIONS:
- Given this history — How would YOU interpret this ECG?
- Which lead is the most concerning?
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| Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
MY Initial Thoughts on Today’s ECG:
The older age of today’s patient — and the fact that he presents to the ED for new CP immediately places this patient in a higher-prevalence risk category (albeit there is some reduction in risk — given the “atypical” nature of his CP). Clearly, more information (ie, assessment of his initial ECG) will be needed for optimal decision-making.
- The initial ECG that is shown in Figure-1 is not normal! That said — the abnormal findings are subtle.
Looking Systematically (as per ECG Blog #205):
- The rhythm is sinus. All intervals (PR, QRS, QTc) are normal. The axis is vertical — but still within normal limits (ie, the QRS is slightly more positive than negative in lead I — so the frontal plane axis is +75-80 degrees). There is no chamber enlargement.
Regarding Q-R-S-T Changes:
- Small and narrow Q waves are seen in the inferior and lateral chest leads (ie, in leads II,III,aVF; and in V5,V6).
- R Wave Progression — is normal, with transition (where the R wave becomes taller than the S wave is deep) taking place normally (seen here in ECG #1 — to be between leads V3-to-V4).
Regarding ST-T Wave Changes:
- PEARL #1: The one lead that immediately "caught my eye" in today's tracing — is lead I (within the RED rectangle in Figure-2). There simply is no way that the ST-T wave in lead I is normal because: i) The ST segment is straightened in lead I (as per the horizontal RED line that I drew over the ST segment in this lead); and, ii) The J-point of this straightened ST segment is depressed (and considering the tiny size of the QRS in lead I — this ST depression is significant!).
- There is subtle-but-real J-point ST elevation in lead III and lead aVF (BLUE arrows in these leads). I was not initially certain of what (if anything) to make of this slight J-point ST elevation in these inferior leads, given the gentle upsloping (ie, "smiley"-configuration) shape and the lack of any J-point ST elevation in the 3rd inferior lead ( = lead II).
- I considered that the symmetric T wave inversion in lead aVL might represent a reciprocal change (BLUE question mark in this lead) — BUT — PEARL #2: The T wave may normally be inverted in lead aVL when the frontal plane axis is vertical, as it is in Figure-2.
- PEARL #3: I considered that the small q waves seen in leads II,III,aVF might represent the injury marker of inferior infarction — but in addition to normal septal q waves being commonly seen in one or more lateral leads (as they are here in leads V5,V6) — normal septal q waves may also normally be seen in the inferior leads when the frontal plane axis is vertical, as it is in Figure-2.
- BOTTOM Line: Were it not for the ST-T wave appearance in lead I — I would not have been at all certain that the above described changes in leads II,III,aVF and aVL were acute, and not simply a manifestation of a repolarization variant in a patient with a vertical frontal plane axis. BUT — Given that I knew that the ST-T wave appearance in lead I was definitely abnormal — My "working diagnosis" was acute inferior OMI until proven otherwise.
PEARL #4: Because of the common blood supply to the inferior and posterior walls of the LV (Left Ventricle) — I always look for subtle signs of acute posterior OMI when I am looking for a way to support my suspicion of acute inferior OMI. Normally — leads V2 and V3 manifest slight-but-real, gently upsloping ST elevation. The fact that if anything — the J-point in lead V3 of ECG #1 is slightly depressed (BLUE arrow in this lead) — strongly suggests that there is an acute posterior OMI in Figure-2.
- NOTE: The more leads that manifest ST-T wave abnormalities — the greater the support that there is an ongoing acute process. My "eye" was next captured by the ST-T wave appearance in leads V4,V5,V6 (within the BLUE rectangle in Figure-2). As per the BLUE lines I've drawn over the ST segments in these leads — there is flattening and slight J-point depression.
- Putting This All Together: Given the history that the older man in today's case presented with new symptoms — and, has ST depression in lead V3 suggestive of posterior OMI — which lends further support to the limb lead changes suggesting inferior OMI — plus also manifesting ST flattening with ST depression in lateral chest leads (V4,V5,V6) — my "working diagnosis" expanded to an acute infero-postero OMI (plus my suspicion that this older patient may well have multivessel disease).
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| Figure-2: I've labeled the initial ECG in today's case. |
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QUESTION:
- Is there misplacement of any electrode leads?
- IF so — WHY is this relevant?
ANSWER:
The only 3 leads that I've not yet mentioned in today's tracing are leads aVR, V1 and V2.
- Lead aVR in Figure-2 — shows slight ST elevation. I thought this finding consistent with the finding of ST depression in lateral leads I; V4,V5,V6 — and possibly indicative of multivessel disease (ie, Diffuse Subendocardial Ischemia — as discussed in ECG Blog #400).
- I strongly suspect that the electrode leads for V1 and V2 may be placed too high on the chest. As discussed in ECG Blog #274 — the clues that suggest there is too-high placement of leads V1,V2 include: i) The negative P wave in leads V1 and V2 of Figure-2; ii) The subtle r' that we see in lead V2; and, iii) How similar the QRST complex in leads V1 and V2 look to the QRST in lead aVR! It is especially this last clue that makes me so suspicious of V1,V2 misplacement — because the symmetric T wave inversion we see in lead V2 looks totally "out-of-place", compared to the ST-T wave appearance in neighboring lead V3 (the BLUE question mark over the T wave in lead V2).
- ST depression with posterior OMI tends to be maximal in leads V2, V3 and/or V4 (with ST depression often beginning in lead V1). Losing the diagnostic utility of leads V1 and V2 in Figure-2 — therefore hinders our ability to recognize posterior OMI in today's patient.
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The CASE Continues:
The clues to acute infero-postero OMI that I discussed above were not recognized.
- Even when several initial high-sensitivity troponin values came back with definite (albeit modest) elevation — the possibility of acute OMI was not recognized.
- The initial ECG was not repeated for several hours ...
- Troponin values continued to rise — and frank ST elevation was finally seen on repeat ECGs.
Additional LESSONS To Be Learned:
ECG findings in Figure-1 are subtle — but they are definitely present. At the least — these ECG changes should have raised concern for a potential acute event.
- When in doubt about an acute event — Repeat the ECG! In acutely evolving coronary occlusion — "dynamic" ST-T wave changes may occur in as short of a time period as several minutes. As a result — I favor repeating ECGs every ~10-20 minutes until you are comfortable that acute OMI is or is not occurring.
- In a patient with new symptoms and subtle ECG changes — the finding of even modest troponin elevation tells us to accept this as evidence of acute OMI until we prove otherwise. Prompt cath is indicated.
- Correlate each serial ECG with notation of the presence and relative severity of symptoms. Improvement of symptoms that correlates with improvement in ECG findings does not mean "all is well". Instead, it most probably indicates "dynamic" ST-T wave changes in a patient with an evolving OMI. Prompt cath and PCI are likely to be needed.
- Even without ECG changes — persistent ischemic-sounding chest pain is indication for prompt cath.
- Finally — the EASIEST way to ensure that you will be able to tell a complete "story" as to the presence and relative severity of symptoms at the time that each ECG was recorded — is if written notation is made on each ECG as it is done on a scale from 0-to-10 of the patient's chest pain at that time.
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Acknowledgment: My appreciation to Giuseppe Trainito (from Butera, Italy) 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" = Occlusion-based 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 (and also Diffuse Subendocardial Ischemia).
- ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).
- ECG Blog #274 — How to tell if leads V1,V2 are misplaced.
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