Written by Magnus Nossen, with edits by Smith
The patient in today's case is a 70-year-old farmer. He has a history of coronary artery disease and a STEMI two years prior that was treated with primary PCI. He contacted EMS due to acute onset chest pain and feeling unwell and fatigued. He was given ASA and sublingual NTG and taken to the ED.
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ECG #2 repeat in the ED. |
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ECG #3 while on NG drip and after morphine |
- T-waves are often dynamic in ACS and may hint at reperfusion and re-occlusion before the ST-segment does.
- In a patient with ACS symptoms disappearing TWI should be considered re-occlusion of the infarct related artery.
- Be careful before administering morphine as it will improve pain.
- T wave inversions are often caused by reperfusion.
Opiates are associated with worse outcomes in Myocardial Infarction.
See this case: A man his 50s with chest pain. What happens when you treat with morphine rather than with reperfusion?
----See this study showing an association between morphine and mortality in ACS:
Use of Morphine in ACS is independently associated with mortality, at odds ratio of 1.4. Meine TJ, Roe M, Chen A, Patel M, Washam J, Ohman E, Peacock W, Pollack C, Gibler W, Peterson E. Association of intravenous morphine use and outcomes in acute coronary syndromes: Results from the CRUSADE Quality Improvement Initiative. Am Heart J. 2005;149:1043–1049.
And Another that we wrote:
65 (23.9%) patients were found to have STEMI(-) occlusion myocardial infarction (OMI) at the time of cardiac catheterization. The 45 patients with STEMI(-) OMI without pre-cath opioids had a door-to-balloon time of 75 minutes, vs. 684 minutes for the 25 STEMI(-) OMI with pre-cath opioids.
High Risk ACS guidelines are only followed in 6% of patiients:
Lupu L, Taha L, Banai A, Shmueli H, Borohovitz A, Matetzky S, Gabarin M, Shuvy M, Beigel R, Orvin K, Minha S ’ar, Shacham Y, Banai S, Glikson M, Asher E. Immediate and early percutaneous coronary intervention in very high-risk and high-risk non-ST segment elevation myocardial infarction patients. Clin Cardiol [Internet]. 2022;Available from: https://onlinelibrary.wiley.com/doi/10.1002/clc.23781
MY Comment, by KEN GRAUER, MD (3/14/2025):
- This all-too-commonly occurring oversight stems from a failure to appreciate the sequential ECG changes that should be expected during the course of an acute evolving infarction.
- The Theory is Simple: Depending on the area of the heart involved — ST segments will elevate with inferior, lateral or anterior OMI when the "culprit" artery occludes — and return to baseline on the way toward T wave inversion when the culprit artery reopens (regardless of whether the artery is reperfused by PCI or thrombolysis — or opens spontaneously).
- The opposite occurs with posterior OMI (ie, there is ST depression with acute occlusion, that is maximal in leads V2,V3,V4 — with return of ST segments to baseline on the way toward developing tall, peaked chest lead T waves that are maximal in leads V2,V3,V4 when the occluded RCA or LCx reopens).
- KEY Point: Correlating each serial ECG to the presence and relative severity of CP at the time each each is done (ie, by a CP "scale" from 1-to-10 that is noted on the chart) — provides an important clue to the state (open or closed) of the "culprit" artery. For example, if posterior reperfusion T waves become less tall and less peaked with a sudden increase in CP severity — this could be a worrisome sign that the "culprit" RCA or LCx is once again occluding (and that ischemic ST depression will soon follow). This fundamental oversight occurred in today's case.
- While delays happen in a busy ED when there are more acute patients than clinicians to care for them — delay should not happen for a higher-risk patient because, “STEMI criteria are not met".
- Along the way — Morphine should not be used to determine if prompt cardiac cath is indicated (as it apparently was in this case). Morphine could have been given early on in today's case — because sudden onset of new CP in a patient with known coronary disease and an obviously abnormal initial ECG is already indication for prompt cath.
- Once you know that prompt cath is needed (because history, ECG findings and troponin indicate acute coronary occlusion) — chest pain relief assumes high priority. But relieving CP before you establish the diagnosis of acute OMI masks symptoms, and only serves to delay the needed PCI (as occurred in today's case).
- As noted by Dr. Nossen, although the initial ECG does not satisfy millimeter-based STEMI criteria — this tracing is markedly abnormal. It is diagnostic of acute postero-lateral OMI. Consistent with the clinical history of reduced CP at the time ECG #1 was recorded — this initial tracing already suggests spontaneous reperfusion because: i) There is deep T wave inversion in lead aVL; ii) The reciprocal of this lead aVL finding is seen in the form of terminal T wave positivity in each of the inferior leads; and, iii) Chest leads show overly tall, T wave peaking that is maximal in leads V2,V3,V4.
- Prove to yourself that there have been dynamic ST-T wave changes. Look lead-to-lead — and compare the relative size of ST-T waves in ECG #1 vs those in ECG #2.
- If you look carefully — Isn't there a difference in ST-T wave appearance in no less than 10/12 leads?
- Although the amount of change in ST-T waves between these 2 tracings may not be great in some leads — the consistency in the direction of these changes is unmistakeable (ie, T wave inversion and T wave peaking are clearly more accentuated in ECG #1 at the time the patient arrived in the ED and CP was decreasing after NTG).
- Isn't there a difference in ST-T wave appearance in virtually all leads?
- Relief of this patient's CP at the time ECG #1 was recorded — is consistent with the above described ECG signs of spontaneous reperfusion of this postero-lateral OMI.
- These reperfusion ST-T wave changes lessened in association with ECG #2 — because this repeat tracing was recorded at a time when CP had returned (ie, on the way toward developing high-lateral lead ST elevation and anterior lead ST depression from postero-lateral OMI).
- ECG #3 reflects further progression of "culprit" artery reocclusion — with ST elevation now clearly beginning in lead aVL — with more acute-looking reciprocal ST depression in inferior leads — and more acute-looking changes across the chest leads.
- Even allowing for failure to recognize acute OMI after ECG #1 — and failure to recognize acute OMI after ECG #2 — awareness of the fundament concept of sequential ECG changes discussed above is essential for the goal of optimizing salvage of viable myocardium (and at least recognizing acute OMI and the need for timely cath from ECG #3).
- The lesson from today's oversights needs to be learned.