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ECG Blog #482 — This Patient got Morphine ...
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The ECG in Figure-1 — was obtained from a man in his 60s, who contacted EMS some time after midnight for new-onset CP (Chest Pain).
- The patient had risk factors, including hypertension, hyperlipidemia, diabetes — and recent episodes of chest discomfort that sounded like angina.
- The patient was hemodynamically stable on arrival of the EMS team. He reported CP severity = 7/10 at the time the initial ECG was recorded.
QUESTIONS:
- How would you interpret the initial ECG in Figure-1?
- — Would you activate the cath lab?
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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 Thoughts on the Initial ECG:
In view of the worrisome history in today’s case, with ongoing severe (7/10) CP — ECG #1 is extremely concerning:
- There is baseline artifact in a number of leads — but the tracing is interpretable.
- The rhythm is sinus at ~85/minute. All intervals (PR,QRS,QTc) are normal. The frontal plane axis is leftward — but not enough to qualify for LAHB (since the QRS in lead II is still predominantly positive). There is no chamber enlargement.
Regarding Q-R-S-T Wave Changes:
- Q Waves — It is hard to know if a Q wave is (or is not) present in lead III (The 1st and 3rd complexes in this lead manifest a small initial r wave — but the middle complex does not).
- R Wave Progression — is normal, with Transition (where the R wave becomes taller than the S wave is deep) occurring normally, here between leads V2-to-V3.
And ST-T Waves?
In this patient with new worrisome CP (still 7/10 at the time ECG #1 was recorded) — there are ST-T wave abns. (abnormalities) in virtually all 12 leads:
- My “eye” was immediately drawn to the 3 leads within the RED rectangle (leads V1,V2,V3 — as shown in Figure-2). There is no LVH in this tracing (ie, No tall R waves in any lateral lead — and no deep S waves in leads V1,V2). Therefore the ST segment straightening with “fatter”-than-expected T wave peak, as well as ~1 mm. of J-point ST elevation in lead V1 is clearly abnormal.
- Considering modest R wave amplitude in lead V2 — the nearly 2 mm. of ST elevation with overly large and “bulky” ST-T waves in this lead also represents a hyperacute change until proven otherwise.
- In the context of leads V1,V2 — the T wave in lead V3 also appears to be “hypervoluminous” ( = hyperacute).
- Flat (if not scooped) ST depression is seen in 2 of the 3 QRST complexes in lateral chest leads V5,V6 (BLUE arrows in these leads).
- Lead V4 is distorted by artifact — but appears to manifest ST segment flattening. It is hard to know what this means given the transition position of lead V3 between the 3 anterior leads (that show ST elevation with hyperacute T waves) — and the 2 lateral chest leads (that show “scooped” ST depression in this patient without ECG indication of LVH).
- In the limb leads — the 2 lateral leads (leads I and aVL) — as well as lead II complement the ST-T wave depression seen in the lateral chest leads (BLUE arrows in these limb leads).
- ST-T waves in leads III and aVF are nonspecific — but manifest ST-T wave flattening.
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MY Impression of ECG #1: In this patient with new and persistent CP — today’s initial ECG strongly suggests acute anteroseptal OMI. This ECG alone (without need for Troponin results) — should prompt the interventionist to take this patient to the cath lab. Unfortunately, this was not done — because the cardiology team felt "STEMI criteria were not met".- See the ADDENDUM below for more on the concept acute OMI (acute MI due to acute coronary Occlusion) — vs the outdated STEMI paradigm. Regardless of whether the initial Troponin value is elevated (The initial Troponin will be normal in a surprising number of patients with acute coronary occlusion) — and regardless of what additional ECGs might show — ECG #1 is diagnostic of acute LAD OMI in this patient with persistent CP until proven otherwise. Prompt cath with PCI is clearly indicated.
- More than just acute LAD OMI — the ECG pattern of hyperacute and elevated ST-T waves in leads V1,V2,V3 + the scooped ST depression in leads V5,V6 — strongly suggests there is Precordial "Swirl" (See below Figure-2).
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| Figure-2: I've labeled today's initial ECG. |
What is Precordial "Swirl"?
As I review in ECG Blog #380 — the colorfully descriptive term known as Precordial Swirl — is an intriguing ECG sign that facilitates recognition of a unique ECG pattern strongly suggestive of a very proximal site of acute LAD occlusion (usually proximal to the 1st septal perforator) — with resultant septal ischemia, in addition to anterior wall and apical involvement.
PEARL #1: In the setting of acute LAD OMI (Occlusion-based MI ) — the pattern of Precordial Swirl is recognized by the finding of ST elevation in lead V1 (and often also in lead aVR) — and — reciprocal ST depression in leads V5 and V6.
- When considering Precordial Swirl — I like to focus on the ST-T wave appearance in leads V1 and V6.
- Although 1-2 mm of upsloping ST elevation is commonly (and normally) seen in anterior leads V2 and V3 — most of the time we do not see ST elevation in lead V1 (or if we do — it is minimal). Therefore — I become immediately suspicious of "Precordial Swirl" whenever there is suggestion of LAD OMI — and — in addition, lead V1 looks different than expected!
- NOTE #1: Sometimes recognition that lead V1 looks "different-than-expected" — is only forthcoming after realizing that lead V2 is clearly abnormal.
- NOTE #2: It's easy to get fooled by LVH! This is because LV "strain" with LVH is sometimes more manifest in anterior rather than lateral chest leads — in which case there may be anterior lead ST elevation (ie, the reciprocal of lateral lead ST-T wave depression). That said — there is no indication of LVH in today's case.
- Finally, once I've decided that the tracing I am looking at is not an example of LVH that mimics Precordial Swirl — I focus my attention on the shape of the ST-T wave in lead V6 (which tends to be flatter, if not scooped — vs the more typical downsloping ST segment of LV "strain").
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The patient was treated en route by the EMS team with ASA and sublingual NTG.
- Following NTG — the patient's CP decreased to 5/10 (from the initial rating of 7/10 CP).
- A repeat ECG was obtained (ECG #2 in Figure-3).
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| Figure-3: The repeat EMS ECG (done ~14 minutes after ECG #1). |
QUESTION:
- How would YOU interpret the repeat ECG in Figure-3?
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PEARL #2:
- Isn't it difficult to assess ECG #2 compared to ECG #1 (that was done ~14 minutes earlier) — without putting both of these ECGs side-by-side?
- Now LOOK at Figure-4 — in which I have placed both of these tracings side-by-side. Isn't it now much easier to go lead-by-lead — in comparing these 2 tracings?
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| Figure-4: Side-by-side comparison between the first 2 EMS ECGs. |
Comparison of Today's Initial ECG — with the Repeat ECG:
Looking lead-by-lead — I noted the following:
- Focusing first on the 3 leads that initially caught my attention (Leads V1,V2,V3 — within the RED rectangle in ECG #1) — there clearly has been deflation of the anteroseptal hyperacute ST-T waves in ECG #2.
- ST depression has clearly decreased in the 5 leads with BLUE arrows in ECG #1.
- PEARL #3: This improvement in ST-T wave morphology in virtually all leads in ECG #2 (compared to ECG #1) — indicates that these are "dynamic" ST-T wave changes. This finding, that occurs in association with decreased severity of the patient's CP — strongly suggests there has been spontaneous reopening of the "culprit" artery.
- BOTTOM Line: If there previously was doubt about the indication for prompt cath in today's case — the finding of dynamic ST-T wave changes in association with reduced CP should have put all doubt to rest.
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The cardiology team still did not want to perform cardiac cath because "STEMI criteria still were not met".
- The patient's CP returned (now 10/10! ) — and a 3rd ECG was done (See side-by-side comparison of the 3 ECGs in today's case in Figure-5).
- Cardiology still did not want to perform cardiac cath.
- Instead — morphine was given for this patient's CP.
QUESTION:
- What do you learn from Figure-5?
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| Figure-5: Side-by-side comparison between ECGs #1,2,3. |
What We Learn from the Serial ECGs in Figure-5:
In Figure-4 — We saw improvement in ECG #2 in virtually all leads, that occurred in association with a reduction in CP.
- Now just 6 minutes later in ECG #3 — the patient's CP has returned to an even more severe degree (10/10 CP! ). The hyperacute ST-T wave changes that we saw in ECG #1 (which had significantly improved at the time ECG #2 was recorded) — have now returned, in association with lateral lead ST depression.
- Relative to QRS amplitude in leads V1-thru-V4 — it appears that T wave size is even greater in these 4 leads compared to ECG #1.
- BOTTOM Line: Recurrence of CP, now increasingly severe — in association with return of acute ST-T wave changes in virtually all leads — strongly suggests that the "culprit" LAD has now spontaneously reclosed.
- Note: This patient's CP has attained a 10/10 intensity despite the administration of morphine. This is not good practice — because often morphine will reduce (relieve) ischemic CP, thereby providing false assurance that the patient is "improving" — when in reality, all the morphine is doing is masking the patient's ischemic symptoms (thereby delaying the need for cardiac cath and definitive treatment).
- PEARL #4: Morphine should only be given after the decision has been made to perform prompt cardiac catheterization. At that point — generous use of morphine for CP relief is welcomed!
- PEARL #5: Morphine could have appropriately been given more than 2 hours earlier had the decision to perform prompt cath been correctly made after seeing ECG #1 (or at latest — after seeing the "dynamic" ST-T wave changes on ECG #2).
- PEARL #6: This final PEARL for today — is essentially a repeat of PEARL #2 — to emphasize how much easier (and how much more time-efficient) it is to compare serial ECGs by putting the tracings you are looking at together, and then going lead-by-lead as you review. There is an "art" to assessment of serial ECGs — as you have to account for potential differences in frontal plane axis, R wave progression (with its effect on QRST morphology), and any change that might result from more or less artifact being present in the lead(s) you are looking at. But can there be any doubt about the "dynamic" ST-T wave changes that we see in Figure-5 that correlate perfectly to the change in relative CP severity?
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Unfortunately — I was unable to obtain full follow-up. But I did find out the following.
- The patient continued to have CP despite morphine and IV NTG. As a result — he was finally taken to cath. This raises the question as to whether this patient would have been taken to cath had the morphine relieved his symptoms!
- The "culprit" artery was confirmed to be the LAD (and given the "Swirl" pattern on ECG — I would bet this was a very proximal LAD lesion).
- Unfortunately — it took nearly 3 hours after ECG #1 until the decision was finally made to perform cardiac catheterization. Time is muscle — so one can only wonder how much potentially viable myocardium was lost by this delay.
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Acknowledgment: My appreciation to Noah Steege (from Virginia, USA) for the case and this tracing.
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ADDENDUM (5/17/2025):
- For More Material — regarding ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria).
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| Figure-6: These are links found in the top menu on every page in this ECG Blog. They lead you to numerous posts with more on OMIs. |
- In "My ECG Podcasts" — Check out ECG Podcast #2 (ECG Errors that Lead to Missing Acute Coronary Occlusion).
- In 'My ECG Videos" — Check out near the top of that page VIDEOS from my MedAll ECG Talks, that review the ECG diagnosis of acute MI — and how to recognize acute OMIs when STEMI criteria are not met (reviewed in ECG Blog #406 — Blog #407 — Blog #408).
- Please NOTE — For each of the 6 MedAll videos at the top of the My ECG Videos page, IF you click on "More" in the description, you'll get a linked Contents that will allow you to jump to discussion of specific points (ie, at 5:29 in the 22-minute video for Blog #406 — you can jump to "You CAN recognize OMI without STEMI findings!" ).
P.S.: For a sobering, thought-provoking case discussed by cardiologist Dr. Willy Frick — with editorial Commentary by me at the bottom of the page (in the March 17, 2025 post) — Check out this case.
- As Dr. Frick and I highlight — not only is the current "STEMI paradigm" outdated — but in cases such as the one we describe, because providers waited until STEMI criteria were finally satisfied — cardiac cath and PCI were delayed for over 1 day.
- BUT — because the cath lab was activated "within 1 hour" of an ECG that finally fulfilled STEMI criteria — this case will go down in study registers as, "highly successful with rapid activation of the cath lab within 1 hour of the identification of a "STEMI". This erroneous interpretation of events totally ignores the clinical reality that this patient needlessly lost significant myocardium because the initial ECG (done >24 hours earlier) was clearly diagnostic of STEMI(-)/OMI(+) that was not acted on because providers were "stuck" on the STEMI protocol.
- The unfortunate result is generation of erroneous literature "support" suggesting validity of an outdated and no longer accurate paradigm.
- The Clinical Reality: Many acute coronary occlusions never develop ST elevation (or only develop ST elevation later in the course) — whereas attention to additional ECG criteria in the above references can enable us to identify acute OMI in many of these STEMI(-) cases at a surprisingly early point in the patient's clinical course.
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