MY Comment, by KEN GRAUER, MD (2/15/2025):
- Failure to recognize posterior OMI is not a problem IF, as often happens — there is clear evidence of associated inferior wall MI (which is common because both the RCA and LCx usually supply both the posterior and inferior walls of the LV). But when infarction is either localized to the posterior wall — or when ECG signs of inferior wall involvement are subtle (as in today’s case) — it becomes easy for the “unaware” provider to overlook posterior OMI.
- Many providers address the lack of ST elevation on a standard ECG by turning to posterior leads. But as we've shown many times in Dr. Smith's ECG Blog — having to pass through the thick back musculature significantly reduces ECG waveform amplitudes, such that the sensitivity of posterior leads for picking up posterior OMI is lacking.
- Posterior leads are not needed to recognize posterior OMI. In a patient with chest pain — the finding of maximal ST segment depression in lead V2 and/or V3 and/or V4 indicates posterior OMI — especially when the shape of such ST segment flattening/depression is consistent with a positive "Mirror" Test (See My Comment in the September 21, 2022 post).
- Because today's patient presented with "ILI" symptoms (ie, of an Influenza-Like Illness) — his chest tightness and diaphoresis was attributed to a viral illness. But all patients who present to an ED with chest discomfort have an ECG — and the initial ECG in today's case (that I've reproduced and labeled in Figure-1) — is diagnostic of acute posterior OMI.
- Today's patient is 84 years old — he has known severe coronary disease (prior CABG; multiple stents) — and he was awakened from sleep because of chest pressure, diaphoresis and light-headedness. Considering this history — any ECG abnormalities have to be assumed acute until proven otherwise.
- Considering this history — my "eye" was immediately drawn to the 2 leads within the RED rectangles. The ST-T wave in lead III is "bulky", coved, ever-so-slightly elevated, and with a hint of terminal T wave inversion. In support that this lead III finding is indicative of acute inferior OMI — is reciprocal ST depression in lead aVL.
- The 2 leads within the BLUE rectangles confirm associated posterior OMI — by the presence of ST segment straightening in lead V2 — and flattened ST depression in lead V3 (whereas normally — there should be slight, gradually upsloping ST elevation in these 2 leads). Especially abnormal are the peaked T waves in these 2 chest leads, with size of the T wave in lead V2 clearly disproportionate to QRS amplitude in V2.
- Other leads (ie, leads II and V6) also manifest T waves that look hyperacute — but despite the artifact — it is the ST-T waves in the 4 leads within the colored rectangles that should indicate acute infero-postero OMI until proven otherwise.
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| Figure-1: Comparison between the first 2 ECGs in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
- Despite the presentation of new severe chest pressure in a high-risk patient — today's initial ECG was not repeated for over 3 hours. Especially when the initial tracing manifests ECG findings of potential concern — the initial ECG should be repeated within no more than 15-30 minutes. Additional serial ECGs should be obtained often until you can be confident of the diagnosis.
- As per Dr. McLaren — a initial negative Troponin does not rule out an acute event, as some time may be needed before Troponin values increase.
- Today's patient became hypotensive following nitroglycerin. Especially when considering acute inferior infarction — NTG-induced hypotension should be a prompt to obtain right-sided leads to rule out significant RV involvement (See My Comment in the July 19, 2020 post).
- Comparison of serial ECGs is best accomplished by placing the 2 tracings being looked at side-by-side. This is done in Figure-1 — and lead-by-lead comparison suggests some of the hyperacute T waves are now not as prominent in the repeat ECG (ie, ST segments have deflated some in leads II,III,aVF) — there is less ST depression in lead aVL — and there has been progression of reperfusion T waves (T wave inversion is now clearly seen in leads III and aVF — and the T wave in lead V2 is taller). If the patient's symptoms were less in association with the development of these reperfusion T waves in ECG #2 — this would be further evidence of acute infero-postero OMI in need of prompt cath.
- BOTTOM Line: If, in a patient with new chest pain — the visual "picture" of ST-T wave flattening-depression in the 2 leads within the BLUE rectangle in Figure-1 is seen — Think acute posterior OMI until proven otherwise. There is no need for posterior leads to arrive at this conclusion.
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Case submitted by Andrew Grimes, Advanced Care paramedic, with additions from Jesse McLaren
An 84-year-old male with a notable cardiac history (CABG, multiple stents) woke at 0500hrs with pressure in his chest, diaphoresis, and light-headedness. He presented to a rural ED at approximately 0630hrs. Since he was recovering from a recent bout of Influenza-like illness and said yes to several ILI screening questions at triage, his chest tightness and diaphoresis were initially attributed to this. Still, an ECG was obtained at 0649hrs:
McLaren: The patient has a high pretest probability based on age, risk factors and symptoms. Influenza-like illness can also trigger plaque rupture. Despite the baseline artifact there’s sinus bradycardia, convex ST elevation in III, reciprocal ST depression in aVL and possible anterior ST depression – indicating inferoposterior OMI. Here’s the Queen of Hearts interpretation, drawing attention especially to III and aVL:
Vitals were grossly normal. He was treated with MDIs, but when this did not provide any improvement, a cardiac workup was ordered. The initial hs-cTn was negative (11 ng/L). He was given two separate sprays of nitroglycerin sublingually, neither of which improved his pain but did cause him to become briefly hypotensive (<90mmHg SBP).
McLaren: it is not unusual for troponin < 2 hours after symptom onset to be in the normal range, which is falsely reassuring in the presence of an ECG showing acute coronary occlusion.
Several hours later, the repeat troponin returned at >600 ng/L. Cardiology at a larger center was consulted and a repeat ECG was obtained at 1119hrs:
McLaren: The inferior T wave inversion suggests either reperfusion (if resolved symptoms) or subacute refractory ischemia – and from the previous description of pain refractory to nitro it is likely the latter. Despite no posterior ST elevation there is still anterior ST depression, and an enlarging R in V2 wave from posterior infarction.
NSTEMI protocol was ordered, and the patient was given ASA, enoxaparin, and ticagrelor. A stat transfer to the cardiology center was ordered. The transfer was uneventful and serial ECGs showed no appreciable further evolution. The patient maintained a 4/10 "pressure" but insisted he was quite comfortable. On arrival at the cardiac care unit, the patient soon underwent PCI. He had a 100% RCA occlusion which was stented. His LCx was open but small, and perfused only a small portion of his posterior wall. The cardiologist described him as a "challenging" case.
I thought this case was interesting with several learning points, including:
1. The initial misdirection to ILI
2. Unrecognized ECG signs of occlusion
3. Treatment as "NSTEMI" despite a 100% RCA occlusion.
4. Regarding the ECG, this case shows inferior ST elevation with reciprocal depression in aVL that does not quite meet STEMI criteria, ST depression maximal in V2-V3 (>97% specific for posterior MI), and an increasingly anterior R wave progression indicating posterior wall infarction.
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